Health Risk and Exposure Assessment for 

Ozone 

Final Report 

 
 

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 EPA-452/R-14-004a 

August 2014 

Health Risk and Exposure Assessment for Ozone 

Final Report 

U.S. Environmental Protection Agency 

Office of Air and Radiation 

Office of Air Quality Planning and Standards 

Health and Environmental Impacts Division 

Risk and Benefits Group 

Research Triangle Park, North Carolina 27711 

 
 

DISCLAIMER

This final document has been prepared by staff from the Risk and Benefits Group, Health and 

Environmental Impacts Division, Office of Air Quality Planning and Standards, U.S. Environmental 

Protection Agency. Any findings and conclusions are those of the authors and do not necessarily reflect 

the views of the Agency. 

 

Questions related to this document should be addressed to Dr. Bryan Hubbell, U.S. 

Environmental Protection Agency, Office of Air Quality Planning and Standards, C539-07, Research 

Triangle Park, North Carolina 27711 (email: hubbell.bryan@epa.gov). 
i 

TABLE OF CONTENTS 

TABLE OF CONTENTS .............................................................................................................. i

LIST OF FIGURES .................................................................................................................... vii

LIST OF TABLES .................................................................................................................... xvii

LIST OF ACRONYMS/ABBREVIATIONS ......................................................................... xxiii

1 INTRODUCTION.......................................................................................................... 1-1

1.1 HISTORY .................................................................................................................. 1-3

1.2 CURRENT RISK AND EXPOSURE ASSESSMENT: GOALS AND PLANNED 

APPROACH .............................................................................................................. 1-6 

1.3 ORGANIZATION OF DOCUMENT ....................................................................... 1-7 

1.4 REFERENCES .......................................................................................................... 1-8 

2 OVERVIEW OF EXPOSURE AND RISK ASSESSMENT DESIGN ..................... 2-1

2.1 POLICY-RELEVANT EXPOSURE AND RISK QUESTIONS .............................. 2-2 

2.2 AIR QUALITY CHARACTERIZATION ................................................................ 2-4 

2.2.1 Ozone Chemistry and Response to Changes in Precursor Emissions .................. 2-5 

2.2.2 Sources of Ozone and Ozone Precursors ............................................................. 2-6 

2.2.3 Simulation of Just Meeting the Existing and Alternative Standards ................... 2-7 

2.3 CONSIDERATION OF HEALTH EVIDENCE ....................................................... 2-8 

2.3.1 Exposures of Concern .......................................................................................... 2-9 

2.3.2 Health Risk Endpoints ....................................................................................... 2-10 

2.3.3 Exposure and Concentration-Response Functions for Health Risk Endpoints .. 2-13 

2.3.4 At-Risk Populations ........................................................................................... 2-15 

2.4 URBAN-SCALE MODELING OF INDIVIDUAL EXPOSURE ........................... 2-16 

2.4.1 Microenvironmental Ozone Concentrations ...................................................... 2-17 

2.4.2 Human Activity Patterns .................................................................................... 2-18 

2.4.3 Modeling of Exposures Associated with Simulating Just Meeting Ozone 

Standards ............................................................................................................ 2-19 

2.4.4 Considerations in Selecting Urban Study Areas for the Exposure Analysis ..... 2-20 

2.5 URBAN- AND NATIONAL-SCALE RISK ASSESSMENT ................................ 2-20 

2.5.1 Attributable Risk ................................................................................................ 2-21 

2.5.2 Modeling of Health Risk Associated with Total Ozone Exposure .................... 2-22 

2.5.3 Distributions of Risk Across Ozone Concentrations ......................................... 2-23 
ii 

2.5.4 Modeling Risk Associated with Simulating Just Meeting Ozone Standards ..... 2-23 

2.5.5 Considerations in Selecting Urban Study Areas for the Risk Assessment ........ 2-24 

2.6 RISK CHARACTERIZATION ............................................................................... 2-24 

2.7 REFERENCES ........................................................................................................ 2-26 

3 SCOPE ............................................................................................................................ 3-1

3.1 OVERVIEW OF THE EXPOSURE AND RISK ASSESSMENTS FROM THE 

LAST REVIEW ......................................................................................................... 3-2 

3.1.1 Overview of Exposure Assessment from the Last Review .................................. 3-2 

3.1.2 Overview of Risk Assessment from the Last Review ......................................... 3-3 

3.2 PLAN FOR THE CURRENT EXPOSURE AND RISK ASSESSMENTS .............. 3-5 

3.3 CHARACTTERIZATION OF UNCERTAINTY AND VARIABILITY IN THE 

CONTEXT OF THE OZONE EXPOSURE AND RISK ASSESSMENT ............... 3-7 

3.4 CHARACTERIZATION OF AIR QUALITY ........................................................ 3-10 

3.5 CHARACTERIZATION OF URBAN-SCALE HUMAN EXPOSURE ................ 3-13 

3.6 CHARACTERIZATION OF URBAN-SCALE HEALTH RISKS BASED ON 

CONTROLLED HUMAN EXPOSURE STUDIES ................................................ 3-15 

3.7 CHARACTERIZATION OF URBAN-SCALE HEALTH RISK BASED ON 

EPIDEMIOLOGICAL STUDIES ........................................................................... 3-18 

3.8 NATIONAL-SCALE MORTALITY RISK ASSESSMENT .................................. 3-21 

3.9 PRESENTATION OF EXPOSURE AND RISK ESTIMATES TO INFORM THE 

OZONE NAAQS POLICY ASSESSMENT ........................................................... 3-24 

3.10 REFERENCES ........................................................................................................ 3-26 

4 AIR QUALITY CHARACTERIZATION .................................................................. 4-1

4.1 INTRODUCTION ..................................................................................................... 4-1 

4.2 OVERVIEW OF OZONE MONITORING AND AIR QUALITY DATA .............. 4-1 

4.3 OVERVIEW OF URBAN-SCALE AIR QUALITY INPUTS TO RISK AND 

EXPOSURE ASSESSMENTS .................................................................................. 4-4 

4.3.1 Urban Study Areas ............................................................................................... 4-5 

4.3.2 Recent Air Quality ............................................................................................... 4-8 

4.3.3 Air Quality Adjustments for Just Meeting Existing and Potential Alternative 

Ozone Standards ................................................................................................ 4-13 

4.4 OVERVIEW OF NATIONAL-SCALE AIR QUALITY INPUTS ......................... 4-30 

4.5 UNCERTAINITIES IN MODELING OF RESPONSES TO EMISSION 

REDUCTIONS TO JUST MEET EXISTING AND POTENTIAL ALTERNATIVE 

STANDARDS.......................................................................................................... 4-37 

4.6 REFERENCES ........................................................................................................ 4-47 

5 CHARACTERIZATION OF URBAN-SCALE HUMAN EXPOSURE ................... 5-1

5.1 SYNOPSIS OF OZONE EXPOSURE AND EXPOSURE MODELING ................. 5-2 

5.1.1 Human Exposure .................................................................................................. 5-2 
iii 

5.1.2 Estimating Ozone Exposure ................................................................................. 5-3 

5.1.3 Modeling Ozone Exposure Using APEX ............................................................ 5-4 

5.2 SCOPE OF THE EXPOSURE ASSESSMENT ........................................................ 5-7 

5.2.1 Urban Areas Selected ........................................................................................... 5-7 

5.2.2 Time Periods Simulated ....................................................................................... 5-9 

5.2.3 Ambient Concentrations Used ............................................................................. 5-9 

5.2.4 Meteorological Data Used ................................................................................. 5-11 

5.2.5 Populations Simulated ....................................................................................... 5-11 

5.2.6 Key Physiological Processes and Personal Attributes Modeled ........................ 5-15 

5.2.7 Microenvironments Modeled ............................................................................. 5-17 

5.2.8 Model Output ..................................................................................................... 5-18 

5.3 EXPOSURE ASSESSMENT RESULTS ................................................................ 5-24 

5.3.1 Overview ............................................................................................................ 5-24 

5.3.2 Exposure Modeling Results for Base Air Quality ............................................. 5-24 

5.3.3 Exposure Modeling Results for Simulations of Just Meeting the Existing and 

Alternative 8-hour Ozone Standards .................................................................. 5-26 

5.4 TARGETED EVALUATION OF EXPOSURE MODEL INPUT AND OUTPUT 

DATA ...................................................................................................................... 5-38 

5.4.1 Analysis of Time-Location-Activity Data ......................................................... 5-38 

5.4.2 Characterization of Factors Influencing High Ozone Exposures ...................... 5-47 

5.4.3 Exposure Results for Additional At-Risk Populations and Lifestages, Exposure 

Scenarios, and Alternative Air Quality Input Data ............................................ 5-49 

5.4.4 Limited Performance Evaluations ...................................................................... 5-57 

5.5 VARIABILITY AND UNCERTAINTY ................................................................. 5-70 

5.5.1 Treatment of Variability .................................................................................... 5-71 

5.5.2 Characterization of Uncertainty ......................................................................... 5-72 

5.6 KEY OBSERVATIONS .......................................................................................... 5-80 

5.7 REFERENCES ........................................................................................................ 5-89 

6 CHARACTERIZATION OF HEALTH RISKS BASED ON CONTROLLED 

HUMAN EXPOSURE STUDIES ................................................................................. 6-1

6.1 INTRODUCTION ..................................................................................................... 6-1 

6.1.1 Development of Approach for Current Risk Assessment .................................... 6-2 

6.1.2 Comparison of Controlled Human Exposure- and Epidemiologic-based Risk 

Assessments ......................................................................................................... 6-3 

6.2 SCOPE OF LUNG FUNCTION HEALTH RISK ASSESSMENT .......................... 6-4 

6.2.1 Selection of Health Endpoints ............................................................................. 6-4 

6.2.2 Approach for Estimating Health Risk Based on Controlled Human Exposure 

Studies .................................................................................................................. 6-5 

6.2.3 Controlled Human Exposure Studies ................................................................... 6-6 
iv 

6.2.4 The McDonnell-Stewart-Smith (MSS) Model ..................................................... 6-9 

6.2.5 The Exposure-Response Function Approach Used in Prior Reviews ............... 6-17 

6.3 OZONE RISK ESTIMATES ................................................................................... 6-22 

6.3.1 Lung Function Risk Estimates Based on the McDonnell-Stewart-Smith 

Model...... ......................................................................................................... 6-23 

6.3.2 Lung Function Risk Estimates Based on the Exposure-Response Functions 

Approach Used in Prior Reviews ....................................................................... 6-29 

6.3.3 Comparison of the MSS Model with the Exposure-Response Function 

Approach... ........................................................................................................ 6-30 

6.4 EVALUATION OF THE MSS MODEL ................................................................ 6-36 

6.4.1 Summary of Published Evaluations ................................................................... 6-36 

6.4.2 Children.............................................................................................................. 6-36 

6.4.3 Threshold vs. Non-Threshold Models ............................................................... 6-37 

6.5 CHARACTERIZATION OF UNCERTAINTY...................................................... 6-38 

6.5.1 Statistical Model Form ....................................................................................... 6-39 

6.5.2 Convergence of APEX Results .......................................................................... 6-44 

6.5.3 Application of Model for All Lifestages ............................................................ 6-45 

6.5.4 Application of Model for Asthmatic Children ................................................... 6-46 

6.5.5 Interaction Between Ozone and Other Pollutants .............................................. 6-46 

6.5.6 2000 vs. 2010 Population Demographics .......................................................... 6-46 

6.5.7 Qualitative Assessment of Uncertainty .............................................................. 6-48 

6.6 KEY OBSERVATIONS .......................................................................................... 6-52 

6.7 REFERENCES ........................................................................................................ 6-56 

7 CHARACTERIZATION OF HEALTH RISK BASED ON EPIDEMIOLOGICAL 

STUDIES ........................................................................................................................ 7-1

7.1 GENERAL APPROACH........................................................................................... 7-1

7.1.1 Basic Structure of the Risk Assessment............................................................... 7-1

7.1.2 Calculating Ozone-Related Health Effects Incidence ........................................ 7-11

7.2 AIR QUALITY CONSIDERATIONS .................................................................... 7-13

7.3 SELECTION OF MODEL INPUTS AND ASSUMPTIONS ................................. 7-15

7.3.1 Selection of Urban Study Areas ......................................................................... 7-15

7.3.2 Selection of Epidemiological Studies and Specification of ConcentrationResponse Functions ........................................................................................... 7-17

7.3.3 Baseline Health Effect Incidence and Prevalence Data ..................................... 7-31

7.3.4 Population (demographic) Data ......................................................................... 7-32

7.4 ADDRESSING VARIABILITY AND UNCERTAINTY ...................................... 7-32

7.4.1 Treatment of Key Sources of Variability ........................................................... 7-35

7.4.2 Qualitative Assessment of Uncertainty .............................................................. 7-40

7.4.3 Description of Core and Sensitivity Analyses ................................................... 7-45
v 

7.5 URBAN STUDY AREA RESULTS ....................................................................... 7-48

7.5.1 Assessment of Health Risk after Adjusting Air Quality to Just Meet the Existing 

Standard ............................................................................................................. 7-65

7.5.2 Assessment of Health Risk after Adjusting Air Quality to Just Meet Alternative 

Standards ............................................................................................................ 7-67

7.5.3 Sensitivity Analyses Designed to Enhance Understanding of the Core Risk 

Estimates ............................................................................................................ 7-72

7.6 KEY OBSERVATIONS .......................................................................................... 7-85

7.7 REFERENCES ........................................................................................................ 7-88

8 CHARACTERIZATION OF NATIONAL-SCALE MORTALITY RISK BASED 

ON EPIDEMIOLOGICAL STUDIES AND AN URBAN-SCALE 

REPRESENTATIVENESS ANALYSIS ...................................................................... 8-1

8.1 NATIONAL-SCALE ASSESSMENT OF MORTALITY RELATED TO OZONE 

EXPOSURE ............................................................................................................... 8-1

8.1.1 Methods................................................................................................................ 8-2

8.1.2 Results .................................................................................................................. 8-6

8.1.3 Sensitivity Analysis ........................................................................................... 8-15

8.1.4 Discussion .......................................................................................................... 8-20

8.2 EVALUATING THE REPRESENTATIVENESS OF THE URBAN STUDY 

AREAS IN A NATIONAL CONTEXT .................................................................. 8-21

8.2.1 Analysis Based on Consideration of National Distributions of Risk-Related 

Attributes............................................................................................................ 8-22

8.2.2 Analysis Based on Consideration of National Distribution of Ozone-Related 

Mortality Risk .................................................................................................... 8-39

8.2.3 Analysis Based on Consideration of National Responsiveness of Ozone 

Concentrations to Emissions Changes ............................................................... 8-43

8.2.4 Discussion .......................................................................................................... 8-65

8.3 REFERENCES ........................................................................................................ 8-66

9 SUMMARY AND SYNTHESIS ................................................................................... 9-1

9.1 INTRODUCTION ..................................................................................................... 9-1

9.2 SUMMARY OF KEY RESULTS ............................................................................. 9-2

9.2.1 Air Quality Considerations .................................................................................. 9-5

9.2.2 Human Exposure Modeling ............................................................................... 9-10

9.2.3 Health Risks Based on Controlled Human Exposure Studies ........................... 9-15

9.2.4 Health Risks Based on Epidemiological Studies (Chapters 7 and 8) ................ 9-19

9.3 COMPARISON OF RESULTS ACROSS EXPOSURE, LUNG FUNCTION RISK, 

AND EPIDEMIOLOGY-BASED MORTALITY AND MORBIDITY RISK 

ANALYSES ............................................................................................................. 9-26

9.3.1 Evaluation of Exposures and Risks after Just Meeting the Existing Standard .. 9-27
vi 

9.3.2 Reductions in Exposure and Risk Metrics after Just Meeting Alternative 

Standards ............................................................................................................ 9-30

9.4 OVERALL ASSESSMENT OF REPRESENTATIVENESS OF EXPOSURE AND 

RISK RESULTS ...................................................................................................... 9-34

9.4.1 Representativeness of Selected Urban Study Areas in Reflecting Area across the 

Nation with Elevated Risk ................................................................................. 9-34

9.4.2 Representativeness of Selected Urban Study Areas in Reflecting Responsiveness 

of Risk to Just Meeting Existing and Alternative O3 Standards ........................ 9-35

9.5 OVERALL ASSESSMENT OF CONFIDENCE IN EXPOSURE AND RISK 

RESULTS ................................................................................................................ 9-37

9.5.1 Uncertainties in Modeling Ozone Responses to Meeting Standards ................. 9-38

9.5.2 Uncertainties in Modeling Exposure and Lung Function Risk .......................... 9-39

9.5.3 Uncertainties in Modeling Epidemiological-Based Risk ................................... 9-39

9.6 OVERALL INTEGREATED CHARACTERIZATION OF RISK IN THE 

CONTEXT OF KEY POLICY RELEVANT QUESTIONS ................................... 9-41

9.7 REFERENCES ........................................................................................................ 9-46

 
vii 

LIST OF FIGURES 

Figure 1-1. Nonattainment Area Classifications Based on the Existing O3 NAAQS. (Source: 

http://www.epa.gov/airquality/greenbook/). ........................................................ 1-2 

Figure 2-1. Overview of Exposure and Risk Assessment Design. ......................................... 2-2 

Figure 2-2. Causal Determinations for O3 Health Effects. ................................................... 2-12 

Figure 3-1. Conceptual Diagram for Air Quality Characterization in the HREA. ............... 3-10 

Figure 3-2. Conceptual Diagram for Population Exposure Assessment. ............................. 3-13 

Figure 3-3. Conceptual Diagram of O3 Lung Function Health Risk Assessment Based on 

Controlled Human Exposure Studies. ................................................................ 3-15 

Figure 3-4. Conceptual Diagram of Urban-Scale Health Risk Assessment Based on Results of 

Epidemiology Studies. ....................................................................................... 3-18 

Figure 3-5. Conceptual Diagram of National O3 Mortality Risk Assessment Based on Results 

of Epidemiology Studies. ................................................................................... 3-22 

Figure 4-1. Map of Monitored 8-hr O3 Design Values for the 2006-2008 Period. ................ 4-3 

Figure 4-2. Map of Monitored 8-hr O3 Design Values for the 2008-2010 Period. ................ 4-3 

Figure 4-3. Flowchart of Air Quality Data Processing for Different Parts of the Urban-scale 

Risk and Exposure Assessments. ......................................................................... 4-4 

Figure 4-4. Trends in Annual 4th Highest Daily Maximum 8-hr Average O3 Concentrations in 

ppb for the 15 Urban Study Areas for 2006-2010. Urban areas are grouped into 3 

regions: Eastern (top), Central (middle), and Western (bottom). ........................ 4-6 

Figure 4-5a. Maps of the 5 Eastern U.S. Urban Study Areas Including O3 Monitor Locations.

........................................................................................................................... .4-10 

Figure 4-6. Flowchart of HDDM Adjustment Methodology to Inform Risk and Exposure 

Assessments. ...................................................................................................... 4-15 

Figure 4-7. Distributions of Composite Monitor Daily Maximum 8-hr Average O3

Concentrations from Ambient Measurements (black), Quadratic Rollback (blue), 

and the HDDM Adjustment Methodology (red) for Meeting the Existing 

Standard. Values are based on the Zanobetti & Schwartz study areas for AprilOctober of 2006-2008. ....................................................................................... 4-22 

Figure 4-8. Distributions of Composite Monitor Daily Maximum 8-hr Average O3

Concentrations from Ambient Measurements (black), Quadratic Rollback (blue), 

and the HDDM Adjustment Methodology (red) for Meeting the Existing 

Standard. Values are based on the Zanobetti & Schwartz study areas for JuneAugust of 2006-2008. ........................................................................................ 4-23 

Figure 4-9. Distributions of Composite Monitor Daily Maximum 8-hr Average Values for the 

12 Urban Study Areas in the Epidemiology-based Risk Assessment. Plots depict 

values based on ambient measurements (base), and values obtained with the 

HDDM adjustment methodology when just meeting the 75, 70, 65 and 60 ppb 

standards. Values shown are based on CBSAs for April-October of 2007. ...... 4-24 
viii 

Figure 4-10. Distributions of Composite Monitor Daily Maximum 8-hr Average Values for the 

12 Urban Study Areas in the Epidemiology-based Risk Assessment. Plots depict 

values based on ambient measurements (base), and values obtained with the 

HDDM adjustment methodology when just meeting the 75, 70, 65 and 60 ppb 

standards. Values shown are based on CBSAs for April-October of 2009... .... 4-25 

Figure 4-11. Maps Showing the 4th highest (top) and May-September Average (bottom) Daily 

Maximum 8-hr Average O3 Concentrations in Atlanta based on 2006-2008 

Ambient Measurements (left), HDDM Adjustment to Meet the Existing Standard 

(center), and HDDM Adjustment to Meet AN Alternative Standard of 65 ppb 

(right). ................................................................................................................ 4-27 

Figure 4-12. Maps Showing the 4th highest (top) and May-September Average (bottom) Daily 

Maximum 8-hr Average O3 Concentrations in New York based on 2006-2008 

Ambient Measurements (left), HDDM Adjustment to Meet the Existing Standard 

(center), and HDDM Adjustment to Meet the Alternative Standard of 65 ppb 

(right).. ............................................................................................................... 4-28 

Figure 4-13. Maps of 4th Highest (top) and May-September Average (bottom) Daily Maximum 

8-hr Average O3 Concentrations in Houston for 2006-2008 Ambient 

Measurements (left), HDDM Adjustment to Meet the Existing Standard (center), 

and HDDM Adjustment to Meet the Alternative Standard of 65 ppb (right).. .. 4-29 

Figure 4-14. May-September Mean of the Daily Maximum 8-hr Average O3 Concentrations in 

ppb, based on a Downscaler Fusion of 2006-2008 Average Monitored Values 

with a 12km 2007 CMAQ Model Simulation.................................................... 4-31 

Figure 4-15. June-August Average 8-hr Daily 10am-6pm Mean O3 Concentrations in ppb, 

based on a Downscaler Fusion of 2006-2008 Average Monitored Values with a 

12km 2007 CMAQ Model Simulation. ............................................................. 4-32 

Figure 4-16. April-September Mean of the Daily Maximum 1-hr O3 Concentrations in ppb, 

based on a Downscaler Fusion of 2006-2008 Average Monitored Values with a 

12km 2007 CMAQ Model Simulation. ............................................................. 4-33 

Figure 4-17. Frequency and Cumulative Distributions of the Three Fused Seasonal Average O3 

Surfaces Based on all CMAQ 12 km Grid Cells. .............................................. 4-34 

Figure 4-18. 2006-2008 O3 Design Values Versus 2006-2008 Fused Seasonal Average O3

Levels for the CMAQ 12km Grid Cells Containing O3 Monitors. .................... 4-36 

Figure 4-19. Propagated Standard Error in Daily Maximum 8-hr Average O3 Concentrations 

Due to Uncertainty in Linear Regression Central Tendency for Each Urban Study 

Area .................................................................................................................... 4-39 

Figure 4-20. Propagated Standard Error in Daily Maximum 8-hr Average O3 Concentrations 

Due to Uncertainty in Linear Regression Central Tendency for Each Urban Study 

Area. Note that this is the same as Figure 4-19 above except with Y-axis adjusted.

............................................................................................................................ 4-40 

Figure 5-1. Conceptual Framework Used for Estimating Study Area Population O3 Exposure 

Concentrations. .................................................................................................... 5-8 

Figure 5-2. Percent of Asthmatic School-age Children in Atlanta with at least One Daily 

Maximum 8-hr Average O3 Exposure while at Moderate or Greater Exertion, 

2006-2010 Air Quality Adjusted to Just Meet the Existing Standard.. ............. 5-21 
ix 

Figure 5-3. Percent of Asthmatic School-age Children in Atlanta with at least One Daily 

Maximum 8-hr Average O3 Exposure while at Moderate or Greater Exertion, 

2006-2010 Air Quality. ...................................................................................... 5-22 

Figure 5-4. Percent of Asthmatic School-age Children in Atlanta with Multiple (≥ 2, ≥ 4, ≥ 6 

per O3 season - red, green, and blue lines) Daily Maximum 8-hr Average O3

Exposures at or above 60 ppb while at Moderate or Greater Exertion, 2006-2010 

Air Quality (x-axes) Adjusted to Just Meet 8-hr O3 Standard Levels of 75, 70, 65, 

60 ppb (panels left to right). ............................................................................... 5-23 

Figure 5-5. Percent of All School-age Children with at Least One Daily Maximum 8-hr 

Average O3 Exposure at or above 60, 70, and 80 ppb (red, green and blue lines) 

while at Moderate or Greater Exertion, 2006-2010 Air Quality Adjusted to Just 

Meet 8-hr Average O3 Standards of 75, 70, 65, and 60 ppb (panels left to right) in 

15 Urban Study Areas. ....................................................................................... 5-31 

Figure 5-6. Percent of Asthmatic School-age Children with at Least One Daily Maximum 8-

hr Average O3 Exposure at or above 60, 70, and 80 ppb (red, green and blue lines) 

while at Moderate or Greater Exertion, 2006-2010 Air Quality Adjusted to Just 

Meet 8-hr Average O3 Standards of 75, 70, 65, and 60 ppb (panels left to right),15 

Urban Study Areas. ............................................................................................ 5-32 

Figure 5-7. Percent of Asthmatic Adults with at Least One Daily Maximum 8-hr Average O3

Exposure at or above 60, 70, and 80 ppb (red, green and blue lines) while at 

Moderate or Greater Exertion, 2006-2010 Air Quality Adjusted to Just Meet 8-hr 

Average O3 Standards of 75, 70, 65, and 60 ppb (panels left to right) in 15 Urban 

Study Areas. ....................................................................................................... 5-33 

Figure 5-8. Percent of Older Adults with at Least One Daily Maximum 8-hr Average O3

Exposure at or above 60, 70, and 80 ppb (red, green and blue lines) while at 

Moderate or Greater Exertion, 2006-2010 Air Quality Adjusted to Just Meet 8-hr 

Average O3 Standards of 75, 70, 65, and 60 ppb (panels left to right) in 15 Urban 

Study Areas. ....................................................................................................... 5-34 

Figure 5-9. Percent of All School-age Children with ≥ 2, ≥ 4, ≥ 6 (red, green, and blue lines) 

Daily Maximum 8-hr Average O3 Exposures at or above 60 ppb while at 

Moderate or Greater Exertion, 2006-2010 Air Quality (x-axes) Adjusted to Just 

Meet 8-hr Average O3 Standards of 75, 70, 65, 60 ppb (panels left to right) in 15 

Urban Study Areas. ............................................................................................ 5-35 

Figure 5-10. Mean Number of People with at Least One Daily Maximum 8-hr Average 

Exposure at or above 60 ppb while at Moderate or Greater Exertion, 2006-2010 

Air Quality Adjusted to Just Meet 8-hr Standards of 75, 70, 65, and 60 ppb (xaxes, from right to left), in 15 Urban Study Areas.. ........................................... 5-36 

Figure 5-11. Mean Number of People with at Least One Daily Maximum 8-hr Average 

Exposure at or above 70 ppb while at Moderate or Greater Exertion, 2006-2010 

Air Quality Adjusted to Just Meet 8-hr Standards of 75, 70, 65, and 60 ppb (xaxes, from right to left), in 15 Urban Study Areas.. ........................................... 5-37 

Figure 5-12. Distribution of Afternoon Time Spent Outdoors for School-age Children on Days 

When Daily Maximum Temperature was ≥ 84 ◦F, Stratified by Four U.S. 

Regions. ............................................................................................................. 5-47 
x 

Figure 5-13. Comparison of the Percent of All School-age Children in Detroit Having Daily 

Maximum 8-hr Average O3 Exposures at or above 60 ppb while at Moderate or 

Greater Exertion, June-August 2007.. ................................................................ 5-50 

Figure 5-14. Percent of Outdoor Workers Ages 19-35 Experiencing Exposures at or above 

Benchmark Levels while at Moderate or Greater Exertion using an Outdoor 

Worker Scenario-based Approach (top panel) and a General Population-based 

Approach (bottom panel), Air Quality Adjusted to Just Meet the Existing 

Standard in Atlanta, GA, Jun-Aug, 2006. .......................................................... 5-52 

Figure 5-15. Percent of All School-age Children (left panel) and Asthmatic School-age 

Children (right panel) Having at Least One Daily Maximum 8-hr Average O3

Exposure at or above Benchmark Levels while at Moderate or Greater Exertion 

During a 2-day Simulation in Detroit, Base Air Quality, August 1-2, 2007. .... 5-54 

Figure 5-16. Comparison of APEX Exposure Results Generated for Three Urban Study Areas 

(Atlanta, Detroit, and Philadelphia) using Three Different 2005 Air Quality Input 

Data Sets: AQS, VNA, and eVNA. ................................................................... 5-55 

Figure 5-17. Comparison of Exposure Results Generated by APEX using Two Different Air 

Quality Adjustment Approaches to Just Meet the Existing Standard in Atlanta: 

Quadratic Rollback (left panel) and HDDM-model Simulation (right panel). .. 5-57 

Figure 5-18. Distribution of Estimated Daily Average O3 Exposures (top panels) and Daily 

Total Outdoor Time (bottom panels) for DEARS Study Adult Participants (left 

panels) and APEX Simulated Adults (right panels) in Wayne County, MI, JulyAugust 2006. ...................................................................................................... 5-58 

Figure 5-19. Distribution of Indoor/Outdoor Concentration Ratios for APEX Simulated Adults 

in Wayne County, MI, July-August 2006. ......................................................... 5-62 

Figure 5-20. Daily Maximum 8-hr Exposures at or above 60 ppb Estimated by APEX for 

Simulated Adults in Wayne County, MI, July-August 2006. ............................ 5-63 

Figure 5-21. Means (and range) of 6-day Average Personal O3 Exposures, Measured and 

Modeled (APEX), Upland Ca.. .......................................................................... 5-64 

Figure 5-22. Comparison of Body Mass Normalized Mean Daily Ventilation Rates Estimated 

by APEX (closed symbols) and by Brochu et al., 2006 (open symbols). .......... 5-66 

Figure 5-23. Comparison of Body Mass Normalized Mean Daily Ventilation Rates in Male and 

Female School-age Children (5-18) when Correcting Brochu et al. (2006a) 

Results with Child Appropriate VQ Estimates. ................................................. 5-67 

Figure 5-24. Comparison of Body Mass Normalized Daily Mean Ventilation Rates in Schoolage Children (5-18) Estimated using APEX and Literature Reported Values. .. 5-68 

Figure 5-25. Incremental Decreases in Percent of All School-age Children Experiencing Daily 

Maximum 8-hr O3 Exposures at or above 60 ppb, with Increasing Stringency in 

Adjusted 2006-2010 Air Quality Standard Levels. ............................................ 5-88 

Figure 6-1. Two-Compartment Model ................................................................................. 6-10 

Figure 6-2. Distribution of Responses (Lung Function Decrements in FEV1) Predicted by the 

MSS Model for 20-Year Old Individuals. Exposure to 100 ppb O3 at Moderate 

Exercise (40 L/min, BSA=2 m2

) Under the Conditions of a Typical 6.6-hour 

Clinical Study..................................................................................................... 6-14 

Figure 6-3. Median Response (Lung Function Decrements in FEV1) Predicted by the MSS 

Model for 20-Year Old Individuals. Exposure to 100 ppb O3 at Moderate Exercise 
xi 

(40 L/min, BSA=2 m2) Under the Conditions of a Typical 6.6-hour Clinical 

Study. ................................................................................................................. 6-15 

Figure 6-4. Median Response (FEV1 Decrements) Predicted by the MSS Threshold and NonThreshold Models for 20-Year Old Individuals, Constant 100 ppb O3 Exposure 

For 6.6 Hours, 2 Hours Heavy Exercise From Hour 1 to 3 (30 L/min-m2

 BSA)...

............................................................................................................................ 6-16 

Figure 6-5. Probability of Response ≥ 10% Predicted by the MSS Threshold and NonThreshold Models for 20-Year Old Individuals, Constant 100 ppb O3 Exposure 

For 6.6 Hours, 2 Hours Heavy Exercise From Hour 1 to 3 (30 L/min-m2

 BSA)...

............................................................................................................................ 6-17 

Figure 6-6. Probabilistic E-R Relationships for FEV1 Decrements ≥ 10% for 8-hr Exposures 

At Moderate Exertion, Ages 18-35. ................................................................... 6-21 

Figure 6-7. Risk Results For All School-Aged Children With ≥ 1 Occurrences of FEV1

Decrements ≥ 10, 15, 20% For All Study Areas, Year, and Scenarios (y-axis is 

percent of children affected). ............................................................................. 6-24 

Figure 6-8. Risk Results For All School-Aged Children With ≥ 1 Occurrences of FEV1

Decrements ≥ 10% Under The 0.07 ppm Alternative Standard Showing 

Variability Across Study Areas (Horizontally) and Years (Vertically). ............ 6-25 

Figure 6-9. Distribution of Daily FEV1 Decrements ≥ 10% Across Ranges of 8-hr Average 

Ambient O3 Concentrations (Los Angeles, 2006 recent air quality). ................ 6-28 

Figure 6-10. Comparison of E-R and MSS Model (restricted to 8-hr average EVR ≥ 13) 

Response Functions (Atlanta 2006 base case, ages 18-35). ............................... 6-34 

Figure 6-11. Distribution of Daily Maximum 8-hr Average EVR For Values of EVR ≥ 13 

(L/min-m2) (midpoints on vertical axis) (Atlanta 2006 base case, ages 18-35). 6-35 

Figure 6-12. Sensitivity (Percent Change) of Population With One or More FEV1 Decrements 

≥ 10% to a 5% Increase in Individual MSS Model Parameter Estimates. ......... 6-41 

Figure 6-13. Lung Function Risk Results, Incremental Increases In Risk For Increasing 

Standard Levels: Percent of All School-aged Children With FEV1 Decrement ≥

10%, Highest Value For Each Study area Over Years ...................................... 6-54 

Figure 6-14. Lung Function Risk Results, Incremental Increases In Risk For Increasing 

Standard Levels: Percent of All School-aged Children With FEV1 Decrement ≥

10%, Mean Value For Each Study Area Over Years ......................................... 6-55 

Figure 7-1. Flow Diagram of Risk Assessment for Short-term Exposure Studies. .............. 7-10 

Figure 7-2. Heat Maps for Short-term O3-attributable Mortality, 2007 Air Quality Adjusted to 

Just Meet the Existing Standard and Risk Reductions from Just Meeting 

Alternative Standards. Smith et al. (2009) C-R functions. ................................ 7-55 

Figure 7-3. Heat Maps for Short-term O3-attributable Mortality, 2009 Air Quality Adjusted to 

Just Meet the Existing Standard and Risk Reductions from Just Meeting 

Alternative Standards. Smith et al. (2009) C-R functions. ................................ 7-56 

Figure 7-4. Short-Term O3-attributable All-Cause Mortality for 2007 (top panel) and 2009 

(bottom panel) Air Quality Adjusted to Just Meet the Existing and Alternative 

Standards. Smith et al. (2009) C-R functions. ................................................... 7-57 

Figure 7-5. Short-Term O3-attributable Respiratory Hospital Admissions, 2007 (top panel) 

and 2009 (bottom panel) Air Quality Adjusted to Meet the Existing and 

Alternative Standards. Medina-Ramon, et al. (2006) C-R functions. ................ 7-61 
xii 

Figure 7-6. Long-Term O3-attributable Respiratory Mortality for 2007 and 2009 Air Quality 

Adjusted to Just Meet the Existing and Alternative Standards, Jerrett et al. (2009) 

C-R functions. .................................................................................................... 7-64 

Figure 7-7. Sensitivity Analysis: Effect of Air Quality Factors on Short-Term O3-attributable 

Mortality, 2009 Air Quality. SA1-smaller (Smith et al., 2009-based) study area, 

SA2-alternative method for simulating standards. ............................................. 7-80 

Figure 7-8. Sensitivity Analysis: Effect of C-R Function Specification on Short-Term O3-

attributable Mortality, 2009 Air Quality. SA1-regional Bayes adjustment, SA2-

co-pollutant model (PM10), SA3-Zanobetti and Schwartz-based function. ....... 7-81 

Figure 7-9. Sensitivity Analysis: Long-Term O3-attributable Respiratory Mortality (threshold 

models: O3-only effect estimates), 2009 Air Quality. ........................................ 7-84 

Figure 8-1. Conceptual Diagram for National-scale Mortality Risk Assessment. ................. 8-2 

Figure 8-2. Estimated Annual non-Accidental Premature Deaths (individuals) in 2007 

Associated with Average 2006-2008 May-September Means of the Daily 

Maximum 8-hr Average O3 Levels by U.S. County using Smith et al. (2009) 

Effect Estimates... ............................................................................................. 8-10 

Figure 8-3. Estimated Annual all-Cause Premature Deaths (individuals) in 2007 Associated 

with Average 2006-2008 June-August Means of the Daily 8-hr Average (10am6pm) O3 Levels by U.S. County using Zanobetti and Schwartz (2008) Effect 

Estimates. ........................................................................................................... 8-10 

Figure 8-4. Estimated Annual Adult (age 30+) Respiratory Premature Deaths (individuals) in 

2007 Associated with Average 2006-2008 April-September Means of the Daily 

Maximum 1-hr O3 Levels by U.S. County using Jerrett et al. (2009) Effect 

Estimates ............................................................................................................ 8-11 

Figure 8-5. Estimated Percentage of May-September Total non-Accidental Mortality (all 

ages) Attributable to 2006-2008 average O3 Levels by U.S. County using Smith et 

al. (2009) Effect Estimates. ................................................................................ 8-11 

Figure 8-6. Estimated Percentage of June-August Total all-Cause Mortality (all ages) 

Attributable to 2006-2008 Average O3 Levels by U.S. County using Zanobetti and 

Schwartz (2008) Effect Estimates. ..................................................................... 8-12 

Figure 8-7. Estimated Percentage of April-September Respiratory Mortality among Adults 

Age 30+ Attributable to 2006-2008 Average O3 Levels by U.S. County using 

Jerrett et al. (2009) Effect Estimates. ................................................................. 8-12 

Figure 8-8. Cumulative Distribution of County-level Percentage of all-cause, all-year, and allage Mortality Attributable to 2006-2008 Average O3 for the U.S. .................... 8-13 

Figure 8-9. Cumulative Percentage of Total O3 deaths by Baseline O3 Concentration. Ozone 

Concentrations are Reported as May-September Mean of the Daily Maximum 8-

hr Average Concentration for Results based on Smith et al. (2009) Effect 

Estimates, June-August Mean of the Daily 8-hr Average (10am to 6pm) for 

Results based on Zanobetti and Schwartz (2008) Effect Estimates, and AprilSeptember Mean of the Daily Maximum 1-hr Concentration for Results based on 

Jerrett et al. (2009) Effect Estimates. ................................................................. 8-14 

Figure 8-10. Seven Regions Used in the Sensitivity Analysis based on the Smith et al. (2009) 

Regional-prior Bayes-shrunken City-specific and Regional Average Effect 

Estimates (Source: Samet et al., 2000). ............................................................. 8-17 
xiii 

Figure 8-11. Ozone-attributable Premature Deaths by Region as Calculated by Applying Smith 

et al. (2009) Regional-prior Bayes-shrunken and Regional-average Effect 

Estimates, as Compared with the National-prior Bayes-shrunken and Nationalaverage Effect Estimates as Done for the Main Results. ................................... 8-18 

Figure 8-12. Comparison of County-level Populations of Urban Study Area Counties to the 

Frequency Distribution of Population in 3,143 U.S. Counties. ......................... 8-31 

Figure 8-13. Comparison of County-level Seasonal Means of the Daily Maximum 8-hr 

Average O3 Concentrations in Urban Study Area Counties to the Frequency 

Distribution of Seasonal Mean of the Daily Maximum 8-hr O3 Concentrations in 

671 U.S. Counties with O3 Monitors.................................................................. 8-31 

Figure 8-14. Comparison of 2007 County-level 4th highest Daily Maximum 8-hr Average O3 

Concentrations in Urban Study Area Counties to the Frequency Distribution of 

2007 4th highest Daily Maximum 8-hr Average O3 Concentrations in 725 U.S. 

Counties with O3 Monitors. ................................................................................ 8-32 

Figure 8-15. Comparison of County-level all-cause Mortality in Urban Study Area Counties to 

the Frequency Distribution of all-cause Mortality in 3,137 U.S. Counties. ...... 8-32 

Figure 8-16. Comparison of County-level non-accidental Mortality in Urban Study Area 

Counties to the Frequency Distribution of non-accidental Mortality in 3,135 U.S. 

Counties ............................................................................................................. 8-33 

Figure 8-17. Comparison of City-level all-cause Mortality Risk Coefficients from Zanobetti 

and Schwartz (2008) in Urban Study Areas to the Frequency Distribution of allcause Mortality Risk Coefficients from Zanobetti and Schwartz (2008) in 48 U.S. 

Cities. ................................................................................................................. 8-33 

Figure 8-18. Comparison of City-level National-prior Bayes-shrunken non-accidental Mortality 

Risk Coefficients from Smith et al. (2009) in Urban Study Areas to the Frequency 

Distribution of National-prior Bayes-shrunken non-accidental Mortality Risk 

Coefficients from Smith et al. (2009) in 98 U.S. Cities ..................................... 8-34 

Figure 8-19. Comparison of County-level Percent of Population 0 to 14 years old in Urban 

Study Area Counties to the Frequency Distribution of Percent of Population 0 to 

14 years old in 3,141 U.S. Counties................................................................... 8-35 

Figure 8-20. Comparison of County-level Percent of Population age 65 years old and older in 

Urban Study Area Counties to the Frequency Distribution of Percent of 

Population age 65 and older in 3,141 U.S. Counties. ........................................ 8-36 

Figure 8-21. Comparison of County-level Income per capita in Urban Study Areas to the 

Frequency Distribution of Income per capita in 3,141 U.S. Counties. .............. 8-36 

Figure 8-22. Comparison of County-level July Temperature in Urban Study Area Counties to 

the Frequency Distribution of July Temperature in all U.S. Counties. .............. 8-37 

Figure 8-23. Comparison of City-level Asthma Prevalence in Urban Study Areas to the 

Frequency Distribution of Asthma Prevalence in 184 U.S. Cities. ................... 8-37 

Figure 8-24. Comparison of City-level Air Conditioning Prevalence in Urban Study Areas to 

the Frequency Distribution of Air Conditioning Prevalence in 76 U.S. Cities.. 8-38 

Figure 8-25. Cumulative Distribution of County-level Percentage of May-September nonaccidental Mortality for all ages Attributable to 2006-2008 Average O3 for the 

U.S. and the Locations of the Selected Urban Study Areas along the Distribution, 

using Smith et al. (2009) Effect Estimates. ........................................................ 8-41 
xiv 

Figure 8-26. Cumulative Distribution of County-level Percentage of June-August all-cause 

Mortality for all ages Attributable to 2006-2008 Average O3 for the U.S. and the 

Locations of the Selected Urban Study Areas along the Distribution, using 

Zanobetti and Schwartz (2008) Effect Estimates. .............................................. 8-42 

Figure 8-27. Cumulative Distribution of County-level Percentage of April-September Adult 

(age 30+) Respiratory Mortality Attributable to 2006-2008 Average O3 for the 

U.S. and the Locations of the Selected Urban Study Areas along the Distribution, 

using Jerrett et al. (2009) Effect Estimates and City Definitions from Zanobetti 

and Schwartz (2008). ......................................................................................... 8-42 

Figure 8-28. Change in 50th Percentile Summer Season (April-October) Daily Maximum 8-hr 

Average O3 Concentrations between 2001-2003 and 2008-2010. ..................... 8-46 

Figure 8-29. Change in 95th Percentile Summer Season (April-October) Daily Maximum 8-hr 

Average O3 Concentrations between 2001-2003 and 2008-2010. ..................... 8-46 

Figure 8-30. Population Density within Census Tract where each O3 Monitor is Located. ... 8-47 

Figure 8-31. Distributions of O3 Concentrations for High Population Density Monitors by 

Different Subsets of Months over a 13-year Period. .......................................... 8-49 

Figure 8-32. Distributions of O3 Concentrations for Medium Population Density Monitors by 

Different Subsets of Months over a 13-year Period. .......................................... 8-49 

Figure 8-33. Distributions of O3 Concentrations for Low Population Density Monitors by 

Different Subsets of Months over a 13-year Period. .......................................... 8-50 

Figure 8-34. Map of O3 Trends at Specific Monitors in the New York Area.. ...................... 8-51 

Figure 8-35. Map of O3 Trends at Specific Monitors in the Chicago Area. All upward and 

downward facing triangles represent statistically significant trends from 1998-

2011 (p < 0.05), circles represent locations with no significant trends.. ........... 8-52 

Figure 8-36. Ratio of April-October Seasonal Average O3 Concentrations in the Brute-force 

50% NOx Emissions Reduction CMAQ Simulations to April-October Seasonal 

Average O3 Concentrations in the 2007 Base CMAQ Simulation. ................... 8-56 

Figure 8-37. Ratio of April-October Seasonal Average O3 Concentrations in the Brute-force 

90% NOx Emissions Reduction CMAQ Simulations to April-October Seasonal 

Average O3 Concentrations in the 2007 Base CMAQ Simulation. ................... 8-56 

Figure 8-38. Ratio of January Monthly Average O3 Concentrations in Brute-force 50% NOx

Emissions Reduction CMAQ Simulations to January Monthly Average O3

Concentrations in the 2007 Base CMAQ Simulation. ....................................... 8-57 

Figure 8-39. Ratio of January Monthly Average O3 Concentrations in Brute-force 90% NOx

Emissions Reduction CMAQ Simulations to January Monthly Average O3

Concentrations in the 2007 Base CMAQ Simulation. ....................................... 8-57 

Figure 8-40. Histograms of U.S. Population Living in Locations with Increasing and 

Decreasing Mean O3 Concentrations. Values on the x-axis represent change in 

mean O3 (ppb) from the 2007 base CMAQ simulation to the 50% NOx cut CMAQ 

simulation.. ......................................................................................................... 8-59 

Figure 8-41. Histograms of U.S. Population Living in Locations with Increasing and 

Decreasing Mean O3 Concentrations. Values on the x-axis represent change in 

mean O3 (ppb) from the 2007 base CMAQ simulation to the 90% NOx cut CMAQ 

simulation.. ......................................................................................................... 8-60 
xv 

Figure 8-42. Population (as % of total case-study area population) Living in Locations of 

Increasing April-October Seasonal Mean O3 in the 50% NOx Reduction CMAQ 

Simulation. ......................................................................................................... 8-61 

Figure 8-43. Population (as % of total case-study area population) Living in Locations of 

Increasing April-October Seasonal Mean O3 in the 90% NOx Reduction CMAQ 

Simulation. ......................................................................................................... 8-61 

Figure 8-44. Histograms of U.S. Population Living in Locations with Increasing and 

Decreasing Mean O3 Concentrations. Values on the x-axis represent the change in 

seasonal mean (April-October) O3 from the 2007 base CMAQ simulation to the 

50% NOx cut CMAQ simulation.. ..................................................................... 8-63 

Figure 8-45. Histograms of U.S. Population Living in Locations with Increasing and 

Decreasing Mean O3 Concentrations. Values on the x-axis represent the change in 

seasonal mean (April-October) O3 from the 2007 base CMAQ simulation to the 

90% NOx cut CMAQ simulation.. ..................................................................... 8-64 

Figure 9-1. Distributions of Composite Monitor Daily Maximum 8-hr Average O3

Concentrations from Ambient Measurements (black), Quadratic Rollback (blue), 

and the HDDM Adjustment Methodology (red) Used for Just Meeting the 

Existing O3 Standard. ........................................................................................... 9-9 

Figure 9-2. Effect of Just Meeting Existing (column 1) and Alternative (columns 2 through 4) 

Standards on the Percent of All School-age Children (ages 5-18) with at Least 

One Daily Maximum 8-hr O3 Exposure at or above 60, 70, and 80 ppb while at 

Moderate or Greater Exertion, 2006-2010 Air Quality. .................................... 9-13 

Figure 9-3. Effect of Just Meeting the Existing (75 ppb) and Alternative Standards on the 

Percent of All School-age Children (ages 5-18) at or above the 60 ppb Exposure 

Benchmark, Maximum Value Across All Years in Each Study Area, 2006-2010 

Air Quality. ........................................................................................................ 9-15 

Figure 9-4. Effect of Just Meeting the Existing (column 1) and Alternative (columns 2-4) 

Standards on the Percent of All School-age Children with FEV1 decrements > 10, 

15, and 20%, 2006-2010 Air Quality. ................................................................ 9-17 

Figure 9-5. Effect of Just Meeting Existing (75 ppb) and Alternative Standards on the Percent 

of All School-age Children (ages 5-18) with FEV1 Decrements ≥ 10%, Maximum 

Value for Each Urban Study Area, 2006-2010 Air Quality. .............................. 9-19 

Figure 9-6. Effect of Just Meeting Existing (75 ppb) and Alternative Standard Levels on 

Mortality Risk per 100,000 Population (left panels) and on Adult (ages 65 and 

older) Respiratory Hospital Admissions Risk per 100,000 Population, 2007 (top 

panels) and 2009 (bottom panels) Air Quality. .................................................. 9-21 

Figure 9-7. Comparison of Exposure (Row 1), Lung Function Risk (Row 2) and 

Epidemiology-Based Risk (Rows 3 and 4) Metrics after Just Meeting the Existing 

75 ppb Standard. ................................................................................................ 9-29 

Figure 9-8. Comparison of the Percent Reduction in Key Risk Metrics for Alternative 

Standard Levels Relative to Just Meeting the Existing 75 ppb Standard. ......... 9-32 
xvi 

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xvii 

LIST OF TABLES 

Table 3-1. Short-term O3 Exposure Health Endpoints Evaluated in Urban Study Areas. .. 3-20 

Table 4-1. Monitor and Area Information for the 15 Urban Study Areas in the Exposure 

Modeling and Clinical Study Based Risk Assessment. ....................................... 4-5

Table 4-2. Monitor and Area Information for the 12 Urban Study Areas in the Epidemiology 

Based Risk Assessment........................................................................................ 4-8

Table 4-3. NOx-only and NOx/VOC Emission Reductions Applied to 15 Urban Study Areas. 

Numbers in blue bold text represent the base scenario while numbers in plain font 

represent the scenario used in the sensitivity analyses for each urban study area...

............................................................................................................................ 4-18

Table 4-4. Summary Statistics based on the Three Fused Seasonal Average O3 Surfaces 

Based on all CMAQ 12 km Grid Cells. ............................................................. 4-35

Table 4-5. Correlation Coefficients between the Three Fused Seasonal Average O3 Surfaces 

Based on all CMAQ 12 km Grid Cells. ............................................................. 4-35

Table 4-6. Correlation Coefficients and Ratios of the 2006-2008 O3 Design Values to the 

2006-2008 Fused Seasonal Average O3 Levels for the CMAQ 12km Grid Cells 

Containing O3 Monitors. .................................................................................... 4-37

Table 4-7. Summary of Qualitative Uncertainty Analysis of Key Air Quality Elements in the 

O3 NAAQS Risk Assessment. ........................................................................... 4-42

Table 5-1. General Characteristics of the Population Exposure Modeling Domain 

Comprising Each Study Area. ............................................................................ 5-10

Table 5-2. Asthma Prevalence for Children and Adults Estimated by APEX in Each 

Simulated Study Area. ....................................................................................... 5-13

Table 5-3. Consolidated Human Activity Database (CHAD) Study Information and Diarydays Used by APEX........................................................................................... 5-14

Table 5-4. Ventilation Equation Coefficient Estimates (bi) and Residuals Distributions (ei)..

............................................................................................................................ 5-16

Table 5-5. Microenvironments Modeled, Calculation Method Used, and Variables Included.

............................................................................................................................ 5-18

Table 5-6. Number and Percent of All CHAD Diaries Used by APEX and Stratified by Four 

U.S. Regions. ..................................................................................................... 5-44

Table 5-7. Number of CHAD Diaries for All School-age Children, Stratified by Four U.S. 

Regions and Diary Pool Attributes. ................................................................... 5-45

Table 5-8. Number and Percent of CHAD Diaries of School-age Children Reporting Time 

Spent Outdoors on Days When Daily Maximum Temperature ≥ 84 ◦F, Stratified 

by Four U.S. Regions, Sex, and Day Type. ....................................................... 5-46

Table 5-9. Percent of All School-age Children with Daily Maximum 8-hr Exposures at or 

above Exposure Benchmarks while at Moderate of Greater Exertion, 2010 Air 

Quality Adjusted to Just Meet the Existing Standard, When Using Either 2000 or 

2010 Census Population Data. ........................................................................... 5-70

Table 5-10. Characterization of Key Uncertainties in Historical and Current Exposure 

Assessments using APEX. ................................................................................. 5-73
xviii 

Table 5-11. Mean and Maximum Percent of all School-age Children Estimated to Experience 

at Least One Daily Maximum 8-hr Average O3 Exposure at or above Selected 

Health Benchmark Levels while at Moderate or Greater Exertion. ................... 5-84

Table 5-12. Mean and Maximum Percent of All School-age Children Estimated to Experience 

at Least Two Daily Maximum 8-hr Average O3 Exposures at or above Selected 

Health Benchmark Levels while at Moderate or Greater Exertion. ................... 5-85

Table 5-13. Mean and Maximum Number of People and Person-days with at Least One Daily 

Maximum 8-hr Average O3 Exposure at or above 60 ppb while at Moderate or 

Greater Exertion for All Exposure Study Groups, All 15 Urban Study Areas 

Combined. .......................................................................................................... 5-87

Table 5-14. Mean and Maximum Number of People and Person-days with at Least One Daily 

Maximum 8-hr Average O3 Exposure at or above 70 ppb while at Moderate or 

Greater Exertion for All Exposure Study Groups, All 15 Urban Study Areas 

Combined. .......................................................................................................... 5-87

Table 6-1. Estimated Parameters in the MSS Models. ........................................................ 6-12

Table 6-2. Age Term Parameters for Application of the 2012 MSS Threshold Model to All 

Ages. .................................................................................................................. 6-13

Table 6-3. Study-specific O3 E-R Data for Lung Function Decrements Based on Correcting 

Individual Responses for the Effect on Lung Function of Exercise in Clean Air, 

Ages 18-35. ........................................................................................................ 6-18

Table 6-4. Ranges of Percents of Population Experiencing One or More and Six or More 

Days during the O3 Season with Lung Function Decrement (∆FEV1) More than 

10%. The numbers in this table are the minimum and maximum percents 

estimated over all study areas and years, for each age group and scenario. ...... 6-26

Table 6-5. Ranges of Percents of Population Experiencing One or More and Six or more 

Days during the O3 Season with Lung Function Decrement (∆FEV1) More than 

15%. The numbers in this table are the minimum and maximum percents 

estimated over all study areas and years, for each age group and scenario. ...... 6-27

Table 6-6. Percents of the General Population and Outdoor Workers (ages 19-35) 

Experiencing One or More and Six or More FEV1 Decrements ≥ 15% (based on 

Atlanta 2006 APEX simulations)....................................................................... 6-29

Table 6-7. Ranges of Percents of all School-aged Children Experiencing One or More Days 

during the O3 Season with Lung Function Decrement (∆FEV1) More than 10 and 

15%, based on the E-R Function Approach. The numbers in this table are the 

minimum and maximum percents estimated over all study areas and years. .... 6-30

Table 6-8. Comparison of Responses from the MSS Model with Responses from the 

Population E-R Method, 2006 Existing Standard Air Quality Scenario, Ages 5 to 

18........................................................................................................................ 6-31

Table 6-9. Comparison of MSS Model and E-R Model of Previous Reviews for Atlanta, Mar 

1-Oct 30, 2006, ages 18-35. ............................................................................... 6-33

Table 6-10. Comparison of MSS Model and E-R Model of Previous Reviews for Los Angeles, 

Jan 1-Dec 31, 2006, ages 18-35. ........................................................................ 6-33

Table 6-11. Comparison of Responses from the MSS 2010 Model with Responses from 

McDonnell et al. (1985). .................................................................................... 6-37
xix 

Table 6-12. Percents of the Population by Age Group with One or More Days during the O3

Season with Lung Function (FEV1) Decrements more than 10, 15, and 20% 

(Atlanta 2006 base case), MSS Threshold Model, Ambient Monitor Data. ...... 6-38

Table 6-13. Percents of the Population by Age Group with One or More Days during the O3

Season with Lung Function (FEV1) Decrements more than 10, 15, and 20% 

(Atlanta 2006 base case), MSS No-Threshold Model, Ambient Monitor Data.....

............................................................................................................................ 6-38

Table 6-14. MSS Threshold Model Estimated Parameters with Confidence Intervals. ........ 6-40

Table 6-15. Sensitivity Analysis of the Inter-individual Variability Term U using the MSS 

Threshold Model. Percents of the population aged 5 to 18 with one or more and 6 

or more days during the O3 season with lung function (FEV1) decrements more 

than 10, 15, and 20% (Atlanta 2006 base case, ambient monitor data). ............ 6-42

Table 6-16. Sensitivity Analysis of the Intra-individual Variability Term ε using the MSS 

Threshold Model. Percents of the population aged 5 to 18 with one or more and 6 

or more days during the O3 season with lung function (FEV1) decrements more 

than 10, 15, and 20% (Atlanta 2006 base case, monitors air quality). ............... 6-44

Table 6-17. Convergence results for the Atlanta 2006 base case with 200,000 simulated 

individuals. Percents of the population by age group with one or more days (and 

six or more days) during the O3 season with lung function (FEV1) decrements 

more than 10, 15, and 20%. Minimum and maximum values and ranges over 40 

APEX runs. ........................................................................................................ 6-45

Table 6-18. Comparison of 2000 vs. 2010 Census Demographics. Percents of all School-aged 

Children (ages 5 to 18) with One or More Days during the O3 Season with Lung 

Function (FEV1) Decrements more than 10, 15, and 20% (7 study areas, 2010 

existing standard air quality). ............................................................................. 6-47

Table 6-19. Comparison of 2000 vs. 2010 Census Demographics. Changes from using 2000 

Demographics to using 2010 Demographics of Percents of all School-aged 

children (ages 5 to 18) with One or More Days during the O3 Season with Lung 

Function (FEV1) Decrements more than 10, 15, and 20% (7 study areas, 2010 

existing standard air quality). ............................................................................. 6-47

Table 6-20. Summary of Qualitative Uncertainties of Key Modeling Elements in the O3 Lung 

Function Risk Assessment ................................................................................. 6-49

Table 7-1. Information on the 12 Urban Study Areas in the Risk Assessment. .................. 7-14

Table 7-2. Overview of Epidemiological Studies Used in Specifying C-R Functions. ...... 7-24

Table 7-3. CBSA-based Study Areas with Multiple Effect Estimates from the Smith et al. 

(2009) Study....................................................................................................... 7-28

Table 7-4. Summary of Qualitative Uncertainty Analysis of Key Modeling Elements in the 

O3 NAAQS Risk Assessment. ........................................................................... 7-42

Table 7-5. Specification of the Core and Sensitivity Analyses (air quality simulation). .... 7-47

Table 7-6. Specification of the Core and Sensitivity Analyses (alternative C-R function 

specification). ..................................................................................................... 7-47

Table 7-7. Short-Term O3-attributable All-Cause Mortality, 2007 and 2009 Air Quality. 

Smith et al. (2009) C-R Functions, O3 season, CBSA-based study area, no 

threshold. ............................................................................................................ 7-53
xx 

Table 7-8. Percent of Total All-Cause Mortality Attributable to O3 and Percent Change in 

O3-Attributable Risk, 2007 and 2009 Air Quality. Smith et al. (2009) C-R 

functions, O3 season, CBSA-based study area, no threshold. ............................ 7-54

Table 7-9. Short-Term O3-attributable Morbidity Counts, Percent of Baseline and Reduction 

in O3-attributable Risk, Respiratory-Related Hospital Admissions, 2007 and 2009 

Air Quality. ........................................................................................................ 7-58

Table 7-10. Short-Term O3-attributable Morbidity Counts, Percent of Baseline and Reduction 

in O3-attributable Risk, Emergency Department Visits, 2007 and 2009 Air 

Quality................................................................................................................ 7-59

Table 7-11. Short-Term O3-attributable Morbidity Counts, Percent of Baseline and Reduction 

in O3-attributable Risk, Asthma Exacerbations, 2007 and 2009 Air Quality. ... 7-60

Table 7-12. Long-Term O3-attributable Respiratory Mortality, 2007 and 2009 Air Quality. 

Jerrett et al. (2009) C-R functions, CBSA-based study area, no threshold. ...... 7-62

Table 7-13. Long-Term O3-attributable Respiratory Mortality Percent of Baseline Incidence 

and Percent Reduction in O3-attributable Risk, 2007 and 2009 Air Quality. Jerrett 

et al. (2009) C-R functions, CBSA-based study area, no threshold. ................. 7-63

Table 7-14. Sensitivity Analysis for Long-Term O3-attributable Respiratory Mortality, 

Alternative C-R Function Specification (regional effect estimates), 2009 Air 

Quality. Percent of baseline all-cause mortality and change in O3-attributable risk, 

Jerrett et al. (2009), O3 season. .......................................................................... 7-82

Table 7-15. Sensitivity Analysis for Long-Term O3-attributable Respiratory Mortality, 

Alternative C-R Function Specification (national O3-only effect estimates), 2009 

Air Quality. Percent of baseline all-cause mortality and change in O3-attributable 

risk, Jerrett et al. (2009), O3 season. .................................................................. 7-83

Table 8-1. Estimated Annual O3-related Premature Mortality in 2007 Associated with 2006-

2008 Average O3 Concentrations (95 percent confidence interval). ................... 8-7

Table 8-2. Mean, Median, 2.5th Percentile, and 97.5th Percentile of the Estimated Percentage 

of Mortality Attributable to Ambient O3 for all 3,109 Counties in the Continental 

U.S. ...................................................................................................................... 8-9

Table 8-3. Sensitivity of Estimated O3-attributable Premature Deaths to the Application of 

the 5th lowest and 5th highest City-specific Risk estimates found by Smith et al. 

(2009) and Zanobetti and Schwartz (2008) to the Grid Cells that do not 

correspond to the Cities Included in Those Studies. .......................................... 8-16

Table 8-4. Sensitivity of Estimated O3-attributable Premature Deaths to the Application of 

Smith et al. (2009) Regional-prior Bayes-shrunken City-specific and Regionalaverage Effect Estimates, as Compared with the National-prior Bayes-shrunken 

City-specific and National-average Effect Estimates as Done for the Main 

Results. ............................................................................................................... 8-16

Table 8-5. Sensitivity of Estimated O3-attributable Premature Deaths to the Application of 

Jerrett et al. (2009) Effect Estimates with and without a Low Concentration 

Threshold. .......................................................................................................... 8-19

Table 8-6. Data Sources for O3 Risk-related Attributes. ..................................................... 8-25

Table 8-7. Summary Statistics for Selected O3 Risk-related Attributes. ............................. 8-28

Table 8-8. Broad Regional Annual Trends of Concurrent O3 Concentrations and Emissions 

of NOx and VOCs over years 2000-2011. ......................................................... 8-53
xxi 

Table 9-1. Summary of Urban Scale O3-Exposure Risk Across Alternative O3 Standard 

Levels. .................................................................................................................. 9-3

Table 9-2. Area and Monitoring Information for the 15 Urban Study Areas. ...................... 9-5

Table 9-3. General Patterns in Seasonal (May-Sept) Mean of Daily Maximum 8-hr O3

Concentrations after Adjusting to Meet Existing and Alternative Standards. ..... 9-7 

 
xxii 

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xxiii 

LIST OF ACRONYMS/ABBREVIATIONS 

AER air exchange rate 

AHRQ Agency for Healthcare Research and Quality 

APEX Air Pollution Exposure Model 

AQI Air Quality Index 

AQS Air Quality System 

ATUS American Time Use Survey 

BenMAP Benefits Mapping and Analysis Program 

BRFSS Behavioral Risk Factor Surveillance System 

BSA body surface area 

CAA Clean Air Act 

CASAC Clean Air Science Advisory Committee 

CASTNET EPA’s Clean Air Status and Trends Network 

CDC Center for Disease Control and Prevention 

CDF cumulative distribution functions 

CH4 methane 

CHAD Consolidated Human Activity Database 

CI confidence interval 

CMAQ Community Multi-scale Air Quality 

CO carbon monoxide 

CO2 carbon dioxide 

COPD chronic obstructive pulmonary disease 

C-R Concentration Response (function) 

DEARS Detroit Exposure and Aerosol Research Study 

DLW doubly-labeled water 

ED emergency department 

EE energy expenditure 

EGU electric generating unit 

EPA U.S. Environmental Protection Agency 

ER emergency room 
xxiv 

E-R Exposure Response (function) 

eVNA enhanced Voronoi Neighbor Averaging 

EVR equivalent ventilation rate 

FEM Federal Equivalent Method 

FEV1 one-second forced expiratory volume 

FRM Federal Reference Method 

FVC forced vital capacity 

HA hospital admissions 

HDDM Higher-order Decoupled Direct Method 

HNO3 nitric acid 

HO2 hydroperoxy radical 

HREA Health Risk and Exposure Assessment 

HUCP Healthcare Cost and Utilization Program 

IPCC Intergovernmental Panel on Climate Change 

IRP Integrated Review Plan 

ISA Integrated Science Assessment 

I/O indoor to outdoor concentration ratio 

LML lowest measured level 

MATS Modeled Attainment Test Software 

ME microenvironment 

METs metabolic equivalents of work 

MSA Metropolitan Statistical Area 

MSS McDonnell-Stewart-Smith model 

MT metric ton 

NAAQS National Ambient Air Quality Standards 

NCDC National Climatic Data Center 

NHANES National Health and Nutrition Examination Survey 

NEI National Emissions Inventory 

NO nitric oxide 

NO2 nitrite 

NOx nitrogen oxides 
xxv 

NRC National Research Council 

O3 Ozone 

OAQPS Office of Air Quality Planning and Standards 

OMB Office of Management and Budget

OH hydroxyl radical 

PA Policy Assessment 

PDI pain on deep inspiration 

PI posterior interval 

PM particulate matter 

ppb parts per billion 

ppm parts per million 

PRB Policy Relevant Background 

REA Risk and Exposure Assessment 

RR relative risk 

SAB Science Advisory Board 

SEDD State Emergency Department Databases 

SES socioeconomic status 

SID State Inpatient Databases 

SO2 sulfur dioxide 

STE stratosphere-troposphere exchange 

TSD technical support document 

TRIM Expo Total Risk Integrated Methodology Inhalation Exposure 

VE ventilation rate 

VNA Voronoi Neighbor Averaging 

VO2 oxygen consumption rate 

VOC volatile organic compound 

VQ ventilatory equivalent 

WHO World Health Organization 

WREA Welfare Risk and Exposure Assessment

 
xxvi 

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1-1 

1 INTRODUCTION 

The U.S. Environmental Protection Agency (EPA) is presently conducting a review of 

the national ambient air quality standards (NAAQS) for ozone (O3), and related photochemical 

oxidants. The NAAQS review process includes four key phases: planning, science assessment, 

risk/exposure assessment, and policy assessment/rulemaking.1 This process and the overall plan 

for this review of the O3 NAAQS is presented in the Integrated Review Plan for the Ozone 

National Ambient Air Quality Standards (IRP; U.S. EPA, 2011a). The IRP additionally presents 

the schedule for the review; identifies key policy-relevant issues; and discusses the key scientific, 

technical, and policy documents. These documents include an Integrated Science Assessment 

(ISA), Risk and Exposure Assessments (REAs), and a Policy Assessment (PA). This Health 

REA (HREA) is one of the two quantitative REAs developed for the review by the EPA’s Office 

of Air Quality Planning and Standards (OAQPS); the second is a Welfare REA (WREA). This 

HREA focuses on assessments to inform consideration of the review of the primary (healthbased) NAAQS for O3. 

The existing primary (health-based) NAAQS for O3 is set at a level of 75 ppb (0.075 

ppm), based on the annual fourth-highest daily maximum 8-hour average concentration, 

averaged over three years, and the secondary standard is identical to the primary standard (73 FR 

16436). Initial nonattainment area designations have been made for 46 areas in the U.S. with 

ambient O3 concentrations exceeding the existing standard (77 FR 30160). For illustrative 

purposes, Figure 1-1 provides the locations of nonattainment areas and their respective 

classifications2 and includes 227 counties with an estimated 2010 population of just over 123 

million people. 

 1

 For more information on the NAAQS review process see http://www.epa.gov/ttn/naaqs/review.html. 2

 Classification thresholds for the 8-hr design value are as follows: marginal (76 to <86 ppb), moderate (86 to <100 

ppb), serious (100 to <113 ppb), severe-15 (113 to <119 ppb), severe-17 (119 to <175 ppb), and extreme (≥175 

ppb). Note that a few nonattainment areas were reclassified to higher classifications following a voluntary request 

by the particular state (77 FR 30160). 
1-2 

Figure 1-1. Nonattainment Area Classifications Based on the Existing O3 NAAQS. 

(Source: http://www.epa.gov/airquality/greenbook/). 

 

The EPA initiated the current review of the O3 NAAQS on September 29, 2008, with an 

announcement of the development of an O3 ISA and a public workshop to discuss policyrelevant science to inform EPA’s integrated plan for the review of the O3 NAAQS (73 FR 

56581). Discussions at the workshop, held on October 29-30, 2008, informed identification of 

key policy issues and questions to frame the review of the O3 NAAQS. Drawing from the 

workshop discussions, the EPA developed a draft and then final IRP (U.S. EPA, 2011a).3 In 

early 2013, the EPA completed the Integrated Science Assessment for Ozone and Related 

Photochemical Oxidants (U.S. EPA, 2013). The ISA provides a concise review, synthesis and 

evaluation of the most policy-relevant science to serve as a scientific foundation for the review 

of the NAAQS. The scientific and technical information in the ISA, including that newly 

available since the previous review on the health effects of O3 includes information on exposure, 

physiological mechanisms by which O3 might adversely impact human health, an evaluation of 

the toxicological and controlled human exposure study evidence, and an evaluation of the 

epidemiological evidence, including information on reported ambient concentration-response (C-

 3

 On March 30, 2009, EPA held a public consultation with the CASAC Ozone Panel on the draft IRP. The final IRP 

took into consideration comments received from CASAC and the public on the draft plan as well as input from 

senior Agency managers. 
1-3 

R) relationships for O3-related morbidity and mortality associations, and also includes 

information on potentially at-risk populations and lifestages.4

This HREA is a concise presentation of the conceptual model, scope, methods, key 

results, observations, and related uncertainties associated with the quantitative analyses 

performed. This HREA builds upon the health effects evidence presented and assessed in the 

ISA, as well as CASAC advice (Samet, 2011), and public comments on a scope and methods 

planning document for the HREA (here after, “Scope and Methods Plan,” U.S. EPA, 2011b). 

Preparation of this HREA draws upon the ISA and reflects consideration of CASAC and public 

comments on the draft HREAs (Frey and Samet, 2012; Frey, 2014). This HREA is being 

released, concurrently with the WREA and PA to inform the proposed O3 NAAQS rulemaking. 

The PA presents a staff evaluation and conclusions of the policy implications of the key 

scientific and technical information in the ISA, and REAs. The PA is intended to help “bridge 

the gap” between the Agency’s scientific assessments presented in the ISA and REAs, and the 

judgments required of the EPA Administrator in determining whether it is appropriate to retain 

or revise the NAAQS. The PA integrates and interprets the information from the ISA and REAs 

to frame policy options for consideration by the Administrator. In so doing, the PA recognizes 

that the selection of a specific approach to reaching final decisions on primary and secondary 

NAAQS will reflect the judgments of the Administrator. The development of the various 

scientific, technical and policy documents and their roles in informing this NAAQS review are 

described in more detail in the PA. 

1.1 HISTORY 

As part of the last O3 NAAQS review completed in 2008, EPA’s OAQPS conducted 

quantitative risk and exposure assessments to estimate exposures above health benchmarks and 

risks of various health effects associated with exposure to ambient O3 in a number of urban study 

areas, selected to illustrate the public health impacts of this pollutant (U.S. EPA 2007a, U.S. 

EPA, 2007b). The assessment scope and methodology were developed with considerable input 

from CASAC and the public, with CASAC generally concluding that the exposure assessment 

reflected generally accepted modeling approaches, and that the risk assessments were well done, 

balanced and reasonably communicated (Henderson, 2006a). The final quantitative risk and 

exposure assessments took into consideration CASAC advice (Henderson, 2006a; Henderson, 

2006b), and public comments on two drafts of the risk and exposure assessments. 

 4

 The ISA also evaluates scientific evidence for the effects of O3 on public welfare which EPA will consider in its 

review of the secondary O3 NAAQS. Building upon the effects evidence presented in the ISA, OAQPS has also 

developed a second REA titled Ozone Welfare Effects Risk and Exposure Assessment (U.S. EPA, 2014). 
1-4 

The exposure and health risk assessment conducted in the last review developed exposure 

and health risk estimates for 12 urban study areas across the U.S., based on 2002 to 2004 air 

quality data. That assessment provided annual or O3 season-specific exposure and risk estimates 

for these years of air quality and for air quality scenarios, simulating just meeting the thenexisting 8-hour O3 standard set in 1997 at a level of 0.08 ppm and several alternative 8-hour 

standards.5 The strengths and limitations in the assessment were characterized, and analyses of 

key uncertainties were presented. 

Exposure estimates from the last assessment were used as an input to the risk assessment 

for lung function responses (a health endpoint for which exposure-response (E-R) functions were 

available from controlled human exposure studies). Exposure estimates were developed for the 

general population and population groups including school-age children with asthma as well as 

all school-age children. The exposure estimates also provided information on exposures to 

ambient O3 concentrations at and above specified benchmark levels (referred to as “exposures of 

concern”), to provide some perspective on the public health impacts of health effects associated 

with O3 exposures in controlled human exposure studies that could not be evaluated in the 

quantitative risk assessment (e.g., lung inflammation, increased airway responsiveness, and 

decreased resistance to infection). For several other health endpoints, O3-related health risk 

estimates were generated using C-R relationships reported in epidemiological or field studies, 

together with ambient air quality concentrations, baseline health incidence rates, and population 

data for the various locations included in the assessment. Health endpoints included in the 

assessment based on epidemiological or field studies included: hospital admissions for 

respiratory illness in four urban study areas, premature mortality in 12 urban study areas, and 

respiratory symptoms in asthmatic children in one urban study area. 

Based on the 2006 Air Quality Criteria for Ozone (U.S. EPA, 2006), the Staff Paper 

(U.S. EPA, 2007c), and related technical support documents (akin to analyses currently 

performed in HREAs), the proposed decision was published in the Federal Register on July 11, 

2007 (72 FR 37818). The EPA proposed to revise the level of the primary standard to a level 

within the range of 0.075 to 0.070 ppm. Two options were proposed for the secondary standard: 

(1) replacing the then-existing standard with a cumulative seasonal standard, expressed as an 

index of the annual sum of weighted hourly concentrations cumulated over 12 daylight hours 

during the consecutive 3-month period within the O3 season with the maximum index value 

(W126), set at a level within the range of 7 to 21 ppm-hours, and (2) setting the secondary 

standard identical to the revised primary standard. The EPA completed the review with 

publication of a final decision on March 27, 2008 (73 FR 16436), revising the level of the 8-hour 

 5

 It is worth noting that the rounding convention applied at that time would allow for design value concentrations to 

include values up to 0.084 ppm and still meet the then-existing standard. 
1-5 

primary O3 standard from 0.08 ppm to 0.075 ppm, as the 3-year average of the fourth highest 

daily maximum 8-hour average concentration, and revising the secondary standard to be 

identical to the revised primary standard. 

Following promulgation of the revised O3 standard in March 2008, state, public health, 

environmental, and industry petitioners filed suit against EPA regarding that final decision. 

At EPA’s request, the consolidated cases were held in abeyance pending EPA’s 

reconsideration of the 2008 decision. A notice of proposed rulemaking to reconsider the 

2008 final decision was issued by the Administrator on January 6, 2010. Three public 

hearings were held. The Agency solicited CASAC review of the proposed rule on January 

25, 2010, and additional CASAC advice on January 26, 2011. On September 2, 2011, the 

Office of Management and Budget (OMB) returned the draft final rule on reconsideration to 

EPA for further consideration. EPA decided to coordinate further proceedings on its 

voluntary rulemaking on reconsideration with this ongoing periodic review, by deferring the 

completion of its voluntary rulemaking on reconsideration until it completes its statutorilyrequired periodic review. In light of that, the litigation on the 2008 final decision proceeded. 

On July 23, 2013, the Court ruled on the litigation of the 2008 decision, denying the 

petitioners suit except with respect to the secondary standard, which was remanded to the 

Agency for reconsideration. The PA provides additional description of the court ruling with 

regard to the secondary standard. 

1.2 CURRENT RISK AND EXPOSURE ASSESSMENT: GOALS AND PLANNED 

APPROACH 

The goals of the current quantitative exposure and health risk assessments are to provide 

information relevant to answering questions regarding the adequacy of the existing O3 standard 

and the potential improvements in public health from meeting alternative standards. To meet 

these goals, this assessment provides results from several analyses, including (1) estimates of the 

number and percent of people in the general population and in at-risk populations and lifestages 

with O3 exposures above benchmark levels, while at moderate or greater exertion levels; (2) 

estimates of the number and percent of people in the general population and in at-risk 

populations and lifestages with impaired lung function resulting from exposures to O3; and (3) 

estimates of the potential magnitude of O3-related premature mortality and selected morbidity 

health effects in the population, including at-risk populations and lifestages, where data are 

available to assess these groups. For each of the analyses, we provide estimates for recent 

ambient levels of O3 and for air quality conditions simulated to just meet the existing O3 standard 

and alternative standards. 
1-6 

In presenting these results, we evaluate the influence of various inputs and assumptions 

on the exposure and risk estimates to more clearly differentiate alternative standards that might 

be considered, including potential impacts on various at-risk populations and lifestages. We also 

evaluate the distribution of risks and patterns of risk reduction and uncertainties in those risk 

estimates. In addition, we have conducted an assessment to provide nationwide estimates of the 

potential magnitude of premature mortality associated with recent ambient O3 concentrations, to 

more broadly characterize this risk on a national scale. This assessment includes an evaluation of 

the distribution of O3-related health risk across the U.S. and associated influential factors, to 

assess the overall representativeness of the risk results generated by our urban study area 

analyses. 

This current quantitative risk and exposure assessment builds on the approach used and 

lessons learned in the last O3 risk and exposure assessment, and focuses on improving the 

characterization of the overall confidence in the exposure and risk estimates, including related 

uncertainties, by incorporating a number of enhancements, in terms of both the models, methods, 

and data used in the analyses. This risk assessment considers a variety of health endpoints for 

which, in staff’s judgment, there is adequate information to develop quantitative risk estimates 

that can meaningfully inform the review of the primary O3 NAAQS. 

1.3 ORGANIZATION OF DOCUMENT 

The remainder of this document is organized as follows. Chapter 2 provides a conceptual 

framework for the risk and exposure assessment, including discussions of O3 chemistry, sources 

of O3 precursors, exposure pathways and microenvironments where O3 exposure can be high, atrisk populations and lifestages, and health endpoints associated with O3. This conceptual 

framework sets the stage for the scope of the risk and exposure assessments. Chapter 3 provides 

an overview of the scope of the quantitative risk and exposure assessments, including a summary 

of the previous risk and exposure assessments, and an overview of the current risk and exposure 

assessments. Chapter 4 discusses the characterization of air quality relevant to the exposure and 

risk assessments, including available O3 monitoring data, and important inputs to the risk and 

exposure assessments. Chapter 5 describes the inputs, models, and results for the urban-scale 

human exposure assessment, and discusses the literature on exposure to O3, the scope of the 

exposure assessment, exposure model inputs, sensitivity and uncertainty evaluations, and 

estimation of results. Chapter 6 describes the estimation of urban-scale health risks based on 

application of the results of controlled human exposure studies combined with the Chapter 5 

exposure results, including discussions of health endpoint selection, approaches to calculating 

risk, and exposure-based risk results. Chapter 7 describes the estimation of health risks in 

selected urban study areas based on application of the results of observational epidemiology 
1-7 

studies, including discussions of air quality characterizations, epidemiological-based risk model 

inputs, variability and uncertainty, and results. Chapter 8 describes the national-scale 

epidemiological-based risk characterization and an urban study area representativeness analysis. 

Chapter 9 provides an integrative discussion of the exposure and risk estimates generated in the 

analyses drawing on the results of the analyses based on both controlled human exposure and 

epidemiological studies, and incorporating considerations from the national-scale risk 

characterization. 

 
1-8 

1.4 REFERENCES 

Frey, C. and J. Samet. 2012. CASAC Review of the EPA’s Health Risk and Exposure Assessment 

for Ozone (First External Review Draft - Updated August 2012) and Welfare Risk and 

Exposure Assessment for Ozone (First External Review Draft - Updated August 2012). U.S. 

Environmental Protection Agency Science Advisory Board. EPA-CASAC-13-002. 

Frey, C. 2014. CASAC Review of the EPA’s Health Risk and Exposure Assessment for Ozone 

(Second External Review Draft – February, 2014). U.S. Environmental Protection Agency 

Science Advisory Board. EPA-CASAC-14-005. 

Henderson, R. 2006a. Clean Air Scientific Advisory Committee (CASAC) Ozone Review 

Panel’s Consultation on EPA’s First Draft Ozone Staff Paper, Risk Assessment, and 

Exposure Assessment Documents. (February, 2006). U.S. Environmental Protection 

Agency Science Advisory Board. EPA-CASAC-CON-06-003. 

Henderson, R. 2006b. Clean Air Scientific Advisory Committee’s (CASAC) Peer Review of the 

Agency’s 2nd Draft Ozone Staff Paper. U.S. Environmental Protection Agency Science 

Advisory Board. EPA-CASAC-07-001. 

Samet, J. 2011. Consultation on EPA’s Ozone National Ambient Air Quality Standards: Scope 

and Methods Plan for Health Risk and Exposure Assessment (April 2011) and Ozone 

National Ambient Air Quality Standards: Scope and Methods Plan for Welfare Risk and 

Exposure Assessment (April 2011). EPA-CASAC-11-008. 

U.S. EPA. 2006. Air Quality Criteria for Ozone and Related Photochemical Oxidants (Final). 

Washington, DC: Office of Research and Development. (EPA document number 

EPA/600/R-05/004aF-cF). 

<http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=149923>. 

U.S. EPA. 2007a. O3 Population Exposure Analysis for Selected Urban Areas. Research 

Triangle Park, NC: Office of Air Quality Planning and Standards. (EPA document 

number EPA-452/R-07-010). 

<http://www.epa.gov/ttn/naaqs/standards/ozone/data/2007_07_o3_exposure_tsd.pdf>. 

U.S. EPA. 2007b. O3 Health Risk Assessment for Selected Urban Areas. Research Triangle Park, 

NC: Office of Air Quality Planning and Standards. (EPA document number EPA 452/R07-009). <http://www.epa.gov/ttn/naaqs/standards/ozone/data/ozone_ra_final_tsd_7-

2007.pdf>. 

U.S. EPA. 2007c. Review of the National Ambient Air Quality Standards for Ozone: Policy 

Assessment of Scientific and Technical Information. OAQPS Staff Paper. Research 

Triangle Park, NC: Office of Air Quality Planning and Standards. (EPA document 

number EPA-452/R-07-007). 

<http://www.epa.gov/ttn/naaqs/standards/ozone/data/2007_07_ozone_staff_paper.pdf>. 

U.S. EPA. 2011a. Integrated Review Plan for the O3 National Ambient Air Quality Standards. 

Research Triangle Park, NC: National Center for Environmental Assessment, Office of 

Research and Development and Office of Air Quality Planning and Standards, Office of 

Air and Radiation. (EPA document number EPA 452/R-11-006). 

<http://www.epa.gov/ttn/naaqs/standards/ozone/data/2011_04_OzoneIRP.pdf>. 

U.S. EPA. 2011b. O3 National Ambient Air Quality Standards: Scope and Methods Plan for 

Health Risk and Exposure Assessment. Research Triangle Park, NC: Office of Air 
1-9 

Quality Planning and Standards. (EPA document number EPA-452/P-11-001). 

<http://www.epa.gov/ttn/naaqs/standards/ozone/data/2011_04_HealthREA.pdf>. 

U.S. EPA. 2013. Integrated Science Assessment of Ozone and Related Photochemical Oxidants 

(Final Report). Research Triangle Park, NC: EPA Office of Research and Development. 

(EPA document number EPA/600/R-10/076F). 

<http://cfpub.epa.gov/ncea/isa/recordisplay.cfm?deid=247492#Download>. 

U.S. EPA. 2014. Welfare Risk and Exposure Assessment for Ozone (Final Report). Research 

Triangle Park, NC: EPA Office of Air and Radiation. (EPA document number EPA452/R-14-005a). 

 
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2-1 

2 OVERVIEW OF EXPOSURE AND RISK ASSESSMENT DESIGN 

In this chapter, we summarize our framework for assessing exposures to O3 and the 

associated risks to human populations. Figure 2-1 provides an overview of the general design of 

this exposure and risk assessment, which includes air quality characterization, review of relevant 

scientific evidence on health effects, modeling of exposure, modeling of risk, and risk 

characterization. Each element identified in the diagram is described in a specific, identified 

chapter of this exposure and risk assessment. 

In this O3 exposure and risk assessment, air quality is characterized primarily by the 

combined use of ambient monitoring data available in EPA Air Quality System (AQS), a spatial 

interpolation approach (Voronoi Neighbor Averaging, VNA), along with Higher-Order 

Decoupled Direct Method (HDDM) capabilities in the Community Multi-scale Air Quality 

(CMAQ)1 model. The modeling of personal exposure and estimation of associated risks based on 

published results from controlled human exposure studies are implemented using the Air 

Pollution Exposure model (APEX; U.S. EPA, 2012 a,b).2

 Modeling of population level risks for 

health endpoints based on application of results reported in published epidemiological studies, is 

implemented using the environmental Benefits Mapping and Analysis Program (BenMAP),3 a 

peer reviewed software tool for estimating risks and impacts associated with changes in ambient 

air quality (U.S. EPA, 2013a). The overall characterization of risk draws from the results of the 

exposure assessment and both types of risk assessment. 

The remainder of this chapter includes summary discussions of each of the main elements 

of Figure 2-1, including policy-relevant exposure and risk questions (Section 2.1), 

characterization of ambient O3, including important sources of O3 precursors, and its relation to 

population exposures, as well as simulation of just meeting existing and potential alternative O3

standards (Section 2.2), review of health evidence identified in the literature describing 

associations with ambient O3 (Section 2.3), key components of exposure modeling (Section 2.4), 

key components of risk modeling (Section 2.5), and risk characterization (Section 2.6). Specific 

details related to the scope of the exposure and risk assessments and how each element will be 

addressed in the quantitative exposure and risk analysis are provided in Chapter 3. 

 

1

 The CMAQ model and associated documentation is available for download at https://www.cmascenter.org/cmaq/. 2

 The APEX model and associated documentation is available for download at 

http://www.epa.gov/ttn/fera/human_apex.html. 3

 The BenMAP model and associated documentation is available for download at http://www.epa.gov/air/benmap/. 
2-2 

Figure 2-1. Overview of Exposure and Risk Assessment Design. 

2.1 POLICY-RELEVANT EXPOSURE AND RISK QUESTIONS 

The first step in the design is to determine the set of policy-relevant exposure and risk 

questions that will be informed by the assessment. Consistent with recommendations from the 

recent National Research Council report “Science and Decisions: Advancing Risk Assessment” 

(NRC, 2009), these exposure and risk assessments have been designed to address the risk 

questions identified in the Integrated Review Plan for the Ozone National Ambient Air Quality 

Standards (IRP; U.S. EPA, 2011). We have focused on designing the exposure and risk 

assessments to inform consideration of those risk-related policy-relevant questions in the 

separately developed O3 NAAQS Policy Assessment (PA; U. S. EPA, 2014). The risk-related 

policy-relevant questions identified in the Integrated Review Plan are related to two main 

activities, evaluation of the adequacy of the existing standards and, if appropriate, evaluation of 
2-3 

potential alternative standards (U.S. EPA, 2011). With regard to evaluation of the adequacy of 

the existing standards, the risk-related policy-relevant questions are: 

“To what extent do risk and/or exposure analyses suggest that exposures of 

concern for O3-related health effects are likely to occur with existing ambient 

levels of O3 or with levels that just meet the O3 standard? Are these 

risks/exposures of sufficient magnitude such that the health effects might 

reasonably be judged to be important from a public health perspective? What are 

the important uncertainties associated with these risk/exposure estimates?” 

With regard to evaluation of potential alternative standards, the risk-related policy-relevant 

questions are: 

“To what extent do alternative standards, taking together levels, averaging times 

and forms, reduce estimated exposures and risks of concern attributable to O3

and other photochemical oxidants, and what are the uncertainties associated with 

the estimated exposure and risk reductions? What conclusions can be drawn 

regarding the health protection afforded at-risk populations?” 

 This risk and exposure assessment is designed to inform consideration of these questions 

through application of exposure and risk modeling for a set of urban study areas. Exposure and 

risk estimates will be generated for recent4

 O3 concentrations, O3 concentrations after simulating 

just meeting the existing standards, and O3 concentrations after simulating just meeting potential 

alternative standards. Careful consideration will be given to addressing variability and 

uncertainty in the estimates, and to the degree to which at-risk populations experience exposures 

and risks. Exposure modeling is discussed in Chapter 5 (Characterization of Urban-Scale Human 

Exposure), while risk modeling is discussed in Chapter 6 (Characterization of Urban-scale 

Health Risk Based on Controlled Human Exposure Studies) and Chapter 7 (Characterization of 

Urban-Scale Health Risk Based on Epidemiological Studies). Chapter 8 (Characterization of 

National-scale Mortality Risk Based on Epidemiological Studies and Urban-Scale 

Representativeness Analysis) provides a national-scale assessment of risks under recent O3

concentrations to provide context for the urban-scale analyses and to help characterize the 

representativeness of the urban-scale analyses. 

In order to inform consideration of the risk-related policy-relevant questions, the first step 

for all of the exposure and risk analyses is simulation of meeting the existing and alternative 

 

4

 To represent recent air quality, the exposure and risk assessments conducted in Chapters 5 to 7 used ambient O3

concentrations from 2006-2010. For risk calculations performed in Chapter 8, data from years 2006-2008 were 

used. 
2-4 

standards. To do this, recent air quality measurements of O3 are adjusted such that they mimic a 

realistic and general atmospheric response to changes in precursor emissions for the specific 

urban study area and so that they just meet the existing and alternative standard levels. 

Conceptually, there is an almost infinite set of combinations of precursor emissions reductions 

that will result in just meeting the existing or alternative standards. The specific combinations of 

reductions that might actually be implemented are not relevant for the exposure and risk 

analyses, as those will result from the implementation processes which follow the establishment 

of a standard. However, it is appropriate to ask the question of how the patterns of ambient O3 on 

multiple temporal scales (hourly, daily, monthly, seasonally) and across each urban study area, 

may respond to precursor emissions reductions that result in meeting the existing and potential 

alternative standards, and how these different patterns of O3 could affect the exposure and risk 

results. The answers to these questions are critical inputs to the exposure and risk analyses. 

Consideration of the available methods for simulating just meeting existing and alternative 

standards is discussed in Chapter 4 (Air Quality Characterization). 

Analyses presented in this document to inform the policy-relevant risk questions 

regarding potential alternative standards, are focused on alternative levels for an 8-hour standard. 

Other elements of the standard (indicator, averaging time, and form),5

 are addressed in the O3 PA 

as part of the overall evaluation of the health protection afforded by the primary O3 standards. 

With regard to potential alternative levels for an 8-hour O3 standard, the quantitative risk 

assessment evaluates the range of levels in 5 ppb increments from 60 to 70 ppb. These levels 

were selected based on the evaluations of the evidence provided in the PA, which received 

support from the CASAC in their advisory letter (Frey and Samet, 2012). For a subset of urban 

study areas, we also evaluated a standard level of 55 ppb, consistent with recommendations from 

CASAC to also give consideration to evaluating a level somewhat below 60 ppb. Thus, for most 

areas, we evaluate exposures and risks for potential alternative standard levels of 70, 65, and 60 

ppb. Some additional analyses were also included for evaluation of exposures and risks for a 

potential alternative 8-hour standard level of 55 ppb. 

2.2 AIR QUALITY CHARACTERIZATION 

In order to address the policy-relevant questions discussed in Section 2.1, the first step is 

characterizing O3 concentrations relevant to estimation of exposure and risk. This requires 

characterization of recent O3 concentrations, O3 concentrations after simulating just meeting the 

 

5

 The “form” of a standard defines the air quality statistic that is compared to the level of the standard in determining 

whether an area attains the standard. The existing form of the 8-hour O3 standard is the 4th highest daily maximum 

8-hour average O3, averaged over 3 years. The “indicator” of a standard defines the chemical species or mixture 

that is to be measured in determining whether an area attains the standard. 
2-5 

existing standards, and O3 concentrations after simulating just meeting potential alternative 

standards. This section provides conceptual information on O3 formation and responsiveness of 

O3 to changes in precursor emissions that inform the simulations of just meeting existing and 

alternative standards. 

2.2.1 Ozone Chemistry and Response to Changes in Precursor Emissions 

Ozone occurs naturally in the stratosphere where it provides protection against harmful 

solar ultraviolet radiation, and it is formed closer to the surface in the troposphere from precursor 

emissions from both natural and anthropogenic sources. Ozone is created when its two primary 

precursors, volatile organic compounds (VOC) and oxides of nitrogen (NOx), combine in the 

presence of sunlight. Volatile organic compounds and NOx are, for the most part, emitted 

directly into the atmosphere. Carbon monoxide (CO) and methane (CH4) can also be important 

for O3 formation (U.S. EPA, 2013b, section 3.2.2). 

Rather than varying directly with emissions of its precursors, O3 changes in a nonlinear 

fashion with the concentrations of its precursors. NOx emissions lead to both the formation and 

destruction of O3, depending on the local concentrations of NOx, VOC, and radicals such as the 

hydroxyl (OH) and hydroperoxy (HO2) radicals. In areas dominated by fresh emissions of NOx, 

these radicals are removed via the production of nitric acid (HNO3), which lowers the O3

formation rate. In addition, the depletion of O3 by reaction with NO is called “titration” and is 

often found in downtown metropolitan areas, especially near busy streets and roads, and in 

power plant plumes. This “titration” results in O3 concentrations that can be much lower than in 

surrounding areas. Titration is usually confined to areas close to strong NOx sources, and the 

NO2 formed can lead to O3 formation later and further downwind. Consequently, O3 response to 

reductions in NOx emissions is complex and may include O3 decreases at some times and 

locations and increases of O3 in other times and locations. In areas with low NOx concentrations, 

such as those found in remote continental areas and rural and suburban areas downwind of urban 

centers, the net production of O3 typically varies directly with NOx concentrations, and increases 

with increasing NOx emissions. 

In general, the rate of O3 production is limited by either the concentration of VOCs or 

NOx, and O3 formation, and using these two precursors relies on the relative sources of OH and 

NOx. When OH radicals are abundant and are not depleted by reaction with NOx and/or other 

species, O3 production is referred to as being “NOx-limited” (U.S. EPA, 2013b, section 3.2.4). In 

this situation, O3 concentrations are most effectively reduced by lowering NOx emissions, rather 

than lowering emissions of VOCs. When the abundance of OH and other radicals is limited 

either through low production or reactions with NOx and other species, O3 production is 

sometimes called “VOC-limited” or “radical limited” or “NOx-saturated” (Jaegle et al., 2001), 
2-6 

and O3 is most effectively reduced by lowering VOCs. However, even in NOx-saturated 

conditions, very large decreases in NOx emissions can cause the O3 formation regime to become 

NOx-limited. Consequently, reductions in NOx emissions (when large), can make further 

emissions reductions more effective at reducing O3. Between the NOx-limited and NOx-saturated 

extremes there is a transitional region, where O3 is less sensitive to marginal changes in either 

NOx or VOCs. In rural areas and downwind of urban areas, O3 production is generally NOxlimited. However, across urban areas with high populations, conditions may vary. For contrast, 

while data from monitors in Nashville, TN, suggest NOx-limited conditions exist there, data from 

monitors in Los Angeles suggest NOx-saturated conditions (U.S. EPA, 2013b, Figure 3-3). 

2.2.2 Sources of Ozone and Ozone Precursors 

Ozone precursor emissions can be divided into anthropogenic and natural source 

categories, with natural sources further divided into biogenic emissions (from vegetation, 

microbes, and animals), and abiotic emissions (from biomass burning, lightning, and geogenic 

sources). The anthropogenic precursors of O3 originate from a wide variety of stationary and 

mobile sources. 

In urban areas, both biogenic and anthropogenic VOCs, as well as CO, are important for 

O3 formation. Hundreds of VOCs are emitted by evaporation and combustion processes from a 

large number of anthropogenic sources. Based on the 2005 national emissions inventory (NEI), 

solvent use and highway vehicles are the two main anthropogenic sources of VOCs, with 

roughly equal contributions to total emissions (U.S. EPA, 2013b, Figure 3-2). The emissions 

inventory categories of “miscellaneous” (which includes agriculture and forestry, wildfires, 

prescribed burns, and structural fires), and off-highway mobile sources are the next two largest 

contributing emissions categories with a combined total of over 5.5 million metric tons a year 

(MT/year). 

On the U.S. and global scales, emissions of VOCs from vegetation are much larger than 

those from anthropogenic sources. Emissions of VOCs from anthropogenic sources in the 2005 

NEI were ~17 MT/year (wildfires constitute ~1/6 of that total), compared to emissions from 

biogenic sources of 29 MT/year. Vegetation emits substantial quantities of VOCs, such as 

isoprene and other terpenoid and sesqui-terpenoid compounds. Most biogenic emissions occur 

during the summer because of their dependence on temperature and incident sunlight. Biogenic 

emissions are also higher in southern and eastern states than in northern and western states for 

these reasons and because of species variations. 

Anthropogenic NOx emissions are associated with combustion processes. Based on the 

2005 NEI, the three largest sources of NOx are on-road and off-road mobile sources (e.g., 

construction and agricultural equipment), and electric power generation plants (EGUs) (U.S. 
2-7 

EPA, 2013b, Figure 3-2). Emissions of NOx therefore are highest in areas having a high density 

of power plants and in urban areas having high traffic density. However, it is not possible to 

make an overall statement about their relative impacts on O3 in all local areas because EGUs are 

sparser than mobile sources, particularly in the west and south and because of the nonlinear 

nature of O3 chemistry discussed in Section 2.2.1. 

Major natural sources of NOx in the U.S. include lightning, soils, and wildfires. Biogenic 

NOx emissions are generally highest during the summer and occur across the entire country, 

including areas where anthropogenic emissions are low. It should be noted that uncertainties in 

estimating natural NOx emissions are much larger than for anthropogenic NOx emissions. 

Ozone concentrations in a region are maintained by a balance between photochemical 

production and transport of O3 into the region; and loss of O3 by chemical reactions, deposition 

to the surface and transport out of the region. Ozone transport occurs on many spatial scales 

including local transport between cities, regional transport over large regions of the U.S. and 

international/long-range transport. In addition, O3 is also transfered into the troposphere from the 

stratosphere, which is rich in O3, through stratosphere-troposphere exchange (STE). 

Stratosphere-troposphere exchange occurs in tropopause “foldings” that occur behind cold 

fronts, bringing stratospheric air with them (U.S. EPA, 2013b, section 3.4.1.1). Contributions to 

O3 concentrations in an area from STE are defined as being part of background O3 (U.S. EPA, 

2013b, section 3.4). 

2.2.3 Simulation of Just Meeting the Existing and Alternative Standards 

Conceptually, simulation of meeting existing and alternative standards should reflect the 

physical and chemical processes of O3 formation in the atmosphere and estimate how hourly 

values of O3 at each monitor in an urban area would change in response to reductions in 

precursor emissions, allowing for nonlinearities in response to emissions reductions and allowing 

for nonlinear interactions between reductions in NOx and VOC emissions. For this assessment, 

we have employed a sophisticated approach (Higher-Order Decoupled Direct Method (HDDM) 

capabilities in the Community Multi-scale Air Quality (CMAQ) model) to conduct simulations 

of hourly O3 responses to reductions in precursor emissions. This modeling incorporates all 

known emissions, including emissions from both natural and anthropogenic sources within and 

outside of the U.S. By using the model-adjustment methodology we are able to more realistically 

simulate the temporal and spatial patterns of O3 response to precursor emissions. We chose to 

simulate just meeting the existing and alternative standards in most cases, by decreasing U.S. 

anthropogenic emissions of NOx exclusively, though in a few instances, proportional decreases 

in both NOx and VOC were applied. This approach, as observed by our modeling, was most 

effective in achieving the desired design values of each air quality scenario and while also 
2-8 

avoiding any suggestion that we are approximating a specific emissions control strategy that a 

state or urban area might adopt to meet a standard. These analyses allow us to apply an 

adjustment to ambient O3 measurements in the urban study areas, to better represent how air 

quality concentrations at each monitor would change to meet the existing and alternative 

standard levels. Furthermore, background O3 concentrations (e.g. that arising from nonanthropogenic emissions) is accounted for by the modeling approach used to simulate each of the 

air quality scenarios, though background O3 concentrations are not separately used in the 

calculation of or in apportioning exposures or health risks. The details of the specific approach 

used to simulating air quality that just meets the existing and alternative standards, are discussed 

in greater detail in Chapter 4 and in the Chapter 4 appendices. 

It is fundamentally a policy decision, as to which sources of precursor emissions are most 

appropriate to decrease to simulate just meeting existing and alternative O3 standards. In 

addressing the policy-relevant questions regarding the evaluation of alternative standards, 

consistent with previous reviews of the O3 standards, this analysis is focused on simulating 

reductions in risk associated with precursor emissions originating from anthropogenic sources 

within the U.S. In doing so, we recognize that the CAA provides mechanisms primarily for 

reducing emissions from U.S. emissions sources. As such, we estimate changes in exposure and 

risks likely to result from just meeting alternative standards relative to just meeting the existing 

standards, by simulating changes in atmospheric concentrations that represent atmospheric 

response to reductions in U.S. anthropogenic emissions. However, we recognize that, in this 

approach, we are simulating air quality that just meets existing and alternative standard levels, 

based on the selected-year air quality concentrations and the chemical environment and 

emissions in these years. We have not mimicked the future-year atmospheric conditions and 

emissions inventory as would be done for the implementation process. 

In addition, while it is possible to decrease O3 concentrations using decreases in either 

NOx or VOC or both NOx and VOC, the specific combination of the reductions in those 

emissions is a policy decision, with recognition that atmospheric chemistry considerations will 

make NOx and VOC decreases more or less effective in specific urban areas, depending on the 

degree to which O3 formation is NOx or VOC limited. As discussed above, in most locations, 

decreases in NOx are the most effective means to decrease ambient O3 concentrations. However, 

in some downtown urban areas, O3 formation is VOC-limited, and therefore smaller decreases in 

NOx will not decrease O3. 

2.3 CONSIDERATION OF HEALTH EVIDENCE 

A critical input for both the exposure and risk assessments is the health evidence 

summarized in the Integrated Science Assessment (ISA; U.S. EPA, 2013b). This health evidence 
2-9 

provides the basis for evaluating the significance of exposures to O3, by informing health 

benchmarks for estimating exposures of concern. The evidence also provides the basis for 

selecting health endpoints that will be modeled in the risk assessment. This evidence includes 

controlled human exposure studies and observational epidemiology studies. The health evidence 

is also the source of the specific studies that are used to develop exposure-response (E-R) and 

concentration-response (C-R) functions, used in the risk assessment. Finally, the health evidence 

provides information on at-risk populations to guide the selections of study populations used in 

the exposure and risk assessments. The following subsections summarize key conceptual aspects 

regarding exposures of concern, health endpoints, E-R and C-R functions, and at-risk 

populations. 

2.3.1 Exposures of Concern 

The O3 ISA identifies health effects associated with exposures to varying concentrations 

of O3. However, not all of the evidence is suitable for evaluation in a quantitative risk 

assessment. Estimating exposures to ambient O3 concentrations at and above benchmark levels 

where health effects have been observed in studies provides a perspective on the public health 

impacts of O3-related health effects that have been demonstrated in human clinical and 

toxicological studies but cannot currently be evaluated in quantitative epidemiological-based 

health risk assessments, such as lung inflammation, increased airway responsiveness, and 

decreased resistance to infection. 

To inform the selection of benchmark levels for O3 exposure, it is appropriate to consider 

the evidence from clinical studies which have evaluated adverse health responses in study 

subjects typically exposed to controlled levels of O3 over 6.6 hours while also engaged in 

moderate quasi-continuous exercise (O3 ISA, section 6.2.1.1). There is substantial evidence from 

these controlled human exposure studies demonstrating a range of O3-related effects including 

lung inflammation and airway responsiveness in healthy individuals at an exposure level of 80 

ppb. There is additional evidence that asthmatics have larger and more serious effects than 

healthy people at 70 ppb, as well as a substantial body of epidemiological evidence of 

associations with O3 levels that extend well below 80 ppb. There is a more limited set of 

evidence based on clinical studies of healthy individuals exposed at 60 ppb in which O3-related 

effects have been observed. This is the lowest level at which any O3-related health effects have 

been observed in clinical studies of healthy individuals (U.S. EPA, 2013b, section 6.2.1.1). 

Thus, estimated exposure concentrations of 60 ppb, 70 ppb, and 80 ppb time-averaged 

over 8 hours in simulated individuals are used in our exposure assessment to indicate exposure 
2-10 

levels of concern (i.e., benchmark levels) for a range of potential health effects in healthy and atrisk populations exposed to O3.

6

2.3.2 Health Risk Endpoints 

The O3 ISA identifies a wide range of health outcomes associated with short-term 

exposure to ambient O3, including an array of morbidity effects as well as premature mortality. 

The ISA also identifies several morbidity effects and some evidence for premature mortality 

associated with longer-term exposures to O3. In identifying health endpoints for risk assessment, 

we have focused on endpoints that pertain to at-risk populations, have public health significance, 

and for which information is sufficient to support a quantitative C-R relationship, in the case of 

epidemiological studies, or E-R relationship, in the case of controlled human exposure studies.7

 

In considering such adverse health effect endpoints for O3, we draw from two types of 

studies: controlled human exposure and epidemiological studies. Each study type informs our 

characterization of O3 risk and can do so in different ways. Estimates of risk based on results of 

controlled human exposure studies are valuable because they provide clear evidence of the 

detrimental effects of controlled (and measured) exposures to O3 over multiple hours on lung 

function at moderate levels of exertion. Results of these studies can be applied to modeled 

estimates of population exposure to provide insights into population exposure characteristics, 

including types of activity patterns and microenvironments that are associated with high levels of 

risk. Controlled human exposure studies, however, cannot directly provide relationships for 

endpoints such as premature death or hospitalizations, focusing more on intermediate biological 

endpoints including inflammatory, blood, neurological, cardiovascular, and respiratory 

biomarkers or symptoms. Further these studies usually do not include particular at-risk subjects 

such as children. Estimates of risk based on C-R functions from observational epidemiology 

studies can provide insights on risk for more serious or chronic health endpoints as well as for 

people at differing lifestages. For example, epidemiological studies of O3 described in the ISA 

have evaluated associations between O3 and various endpoints including respiratory symptoms, 

respiratory-related hospitalizations and emergency department (ED) visits, and premature 

 

6

 Note that the existing and potential alternative ambient standards that are evaluated using this assessment 

approach, regardless of the level, averaging time, and form of the standard are designed to limit exposures based 

on these controlled exposure concentrations of 60, 70, and 80 ppb that were evaluated in the clinical studies. This 

is not to say that there are not health effects that could occur with exposures within the range of these benchmark 

levels (e.g., an 8-hour average exposure of 75 ppb) but that responses occurring at any alternative exposure 

concentrations have not been directly assessed in the clinical studies. 7

 The distinction between C-R and E-R functions reflects the typical use of ambient concentrations as measured at 

monitor locations as surrogates for population exposures in observational epidemiology studies, as compared to 

the personal exposures to controlled concentrations of O3 that are typically used in controlled human exposure 

studies. Both types of studies are intended to produce an E-R relationship, however, the epidemiology studies are 

actually providing a C-R relationship, which captures the E-R relationship with errors in exposure measurement. 
2-11 

mortality (U.S. EPA, 2013b, sections 6.2.9 and 6.3.4). Epidemiological studies also generally 

focus on a population residing in specific area, which may reflect a broad range of 

susceptibilities and sensitivities. Controlled human exposure studies typically involve a smaller 

number of individuals over a more limited range of health status, in some cases focused on atrisk populations, such as asthmatics and individuals with chronic obstructive pulmonary disease 

(COPD). Lastly, while controlled human exposure studies directly measure the exposures 

eliciting the recorded effects, epidemiology studies have not traditionally been based on 

observations of personal exposure to ambient O3, relying instead on surrogate measures of 

population exposure. Such surrogates are often based on simple averages of ambient O3 monitor 

observations. Thus, with attention to their differing strengths and limitations, risk analyses based 

on each type of study can inform the risk characterization. 

The O3 ISA makes overall causal determinations based on the full range of evidence 

including epidemiological, controlled human exposure, and toxicological studies. Figure 2-1 

shows the O3 health effects which have been categorized by strength of evidence for causality in 

the O3 ISA (U.S. EPA, 2013b, chapter 2). The health evidence supporting each of these three 

categories considered here are defined briefly: 

 Causal: Health effect evidence is sufficient to conclude that there is a causal relationship 

with relevant pollutant exposures. That is, the pollutant has been shown to result in health 

effects in studies in which chance, bias, and confounding could be ruled out with 

reasonable confidence.

 Likely: Evidence is sufficient to conclude that a causal relationship is likely to exist with 

relevant pollutant exposures, but important uncertainties remain. That is, the pollutant has 

been shown to result in health effects in studies in which chance and bias can be ruled out 

with reasonable confidence but potential issues remain.

 Suggestive: Evidence is suggestive of a causal relationship with relevant pollutant 

exposures, but is limited.

The O3 ISA determined there are causal relationships between short-term exposure to 

ambient O3 and respiratory effects, including respiratory-related morbidity and mortality and a 

likely causal relationship with all-cause total mortality and with cardiovascular effects; the 

evidence was concluded to be suggestive of a causal relationship between short-term exposure to 

ambient O3 and central nervous system effects. The ISA determined to also be a likely causal 

relationship between long-term O3 exposures and respiratory effects (including respiratory 

symptoms, new-onset asthma, and respiratory mortality), and determined the evidence to be 

suggestive of causal relationships between long-term O3 exposures and total mortality as well as 

cardiovascular, reproductive and developmental, and central nervous system effects. 
2-12 

Figure 2-2. Causal Determinations for O3 Health Effects. 

The ISA identifies several specific respiratory responses to short-term O3 exposure that 

have been evaluated in controlled human exposure studies (U.S. EPA, 2013b, section 6.2.1). 

These include decreased inspiratory capacity, decreased forced vital capacity (FVC) and forced 

expiratory volume in 1 second (FEV1); mild bronchoconstriction; rapid, shallow breathing 

patterns during exercise; symptoms of cough and pain on deep inspiration (PDI); and pulmonary 

inflammation. While such studies document quantitative relationships between short-term O3

exposure and an array of respiratory-related effects, E-R data across a range of concentrations 

sufficient for developing quantitative risk estimates are only available for O3-related decrements 

in FEV1 (U.S. EPA, 2013b, section 6.2.1). 

Within the broad category of respiratory morbidity effects, the epidemiology literature 

has provided effect estimates for a wide range of health endpoints associated with short-term O3 

exposures which we have considered for risk assessment. These health endpoints include lung 

function, respiratory symptoms and medication use, respiratory-related hospital admissions, and 

emergency department visits. In the case of respiratory symptoms, the evidence is most 

consistently supportive of the relationship between short-term ambient O3 metrics and Long‐term

O3 exposures

Cardiovascular effects

Total Mortality

Respiratory effects

Cardiovascular effects

Total Mortality Respiratory effects

Central nervous

system effects

Reproductive and

developmental effects

Central nervoussystem

effects

Short‐term

O3 exposures

Suggestive Likely Causal
2-13 

respiratory symptoms and asthma medication use in children with asthma, but not for a 

relationship between O3 and respiratory symptoms in children without asthma (U.S. EPA, 2013b, 

section 6.2.9). In the case of hospital admissions, there is evidence of associations between shortterm ambient O3 metrics and general respiratory-related hospital admissions as well as more 

specific asthma-related hospital admissions (U.S. EPA, 2013b, section 6.2.7.2). 

With regard to mortality, studies have evaluated associations between short-term ambient 

O3 metrics and all-cause, non-accidental, and cause-specific (usually respiratory or 

cardiovascular) mortality. The evidence from respiratory-related morbidity studies provides 

strong support for respiratory-related mortality for which a causal determination has been made 

(U.S. EPA, 2013b, Table 2-3). There are also a number of large studies that have found 

associations between O3 and all-cause and all non-accidental mortality for which a likely causal 

determination has been made (U.S. EPA, 2013b, Table 2-3). Thus, it is appropriate to assess 

risks for respiratory-related mortality as well as for all-cause total mortality associated with O3

exposure. The ISA also reports a likely causal determination for short-term O3 and 

cardiovascular effects, including cardiovascular mortality (U.S. EPA, 2013b, Table 2-3). This 

determination is supported by studies relating total and cardiovascular mortality, coupled with 

evidence from animal toxicological studies and controlled human exposure studies which find 

effects of O3 on systemic inflammation and oxidative stress. Cardiovascular mortality effects are 

covered through the estimation of risks associated with total mortality, which is dominated by 

cardiovascular mortality. There are not sufficient epidemiological studies of cardiovascular 

morbidity showing consistent associations to justify inclusion of any cardiovascular morbidity 

endpoints in the quantitative risk assessment. 

With regard to effects associated with long-term O3 exposures, the ISA states that the 

relationship between O3 and respiratory-related effects, including respiratory symptoms, newonset asthma, and respiratory mortality is likely causal (U.S. EPA, 2013b, Table 2-3). This 

suggests that for long-term exposures, when comparing the evidence for respiratory-related 

mortality and total mortality, the evidence is strongest for respiratory-related mortality, which is 

supported by the strong evidence for respiratory morbidity. As a result, it is appropriate to 

include respiratory mortality rather than total mortality in the risk assessment and to give 

consideration to inclusion of additional respiratory-related health endpoints. 

2.3.3 Exposure and Concentration-Response Functions for Health Risk Endpoints 

Estimation of risk requires characterization of the E-R and C-R functions along the full 

range of potential exposures. For E-R functions, the evidence from individual controlled human 

exposure studies provides responses for exposures at and above 60 ppb. McDonnell et al. (2012) 

develop an integrated model of FEV1 response that is fit to the results from controlled human 
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exposure studies and find that a model with a threshold provides the best fit to the data. In 

addition, the ISA notes that it is difficult to characterize the E-R relationship at and below 40 ppb 

due to the dearth of data at these lower concentrations (U.S. EPA, 2013b, section 2.5.4.4). Thus, 

for the portion of the risk assessment based on application of results of controlled human 

exposure studies, the threshold model is applied. 

The evidence for a threshold in the C-R functions for mortality and morbidity outcomes 

derived from the epidemiological literature is limited. In general, the epidemiological evidence 

suggests a generally linear C-R function with no indication of a threshold. However, evaluation 

of evidence for a threshold in the C-R function is complicated by the high degree of 

heterogeneity between cities in the C-R functions and by the sparse data available at lower 

ambient O3 concentrations (U.S. EPA, 2013b, sections 2.5.4.4 and 2.5.4.5). 

The ISA also evaluated whether the magnitude of the relationship between short-term 

exposures to O3 and mortality changes at lower concentrations (e.g., whether the C-R function is 

non-linear). The ISA concludes that epidemiologic studies that examined the shape of the C-R 

curve and the potential presence of a threshold have indicated a generally linear C-R function 

with no indication of a threshold in analyses that have examined 8-hour max and 24-hour 

average O3 concentrations, and that the evidence supports less certainty in the shape of the C-R 

function at the lower end of the distribution of O3 concentrations, e.g., 24-hour average O3 below 

20 ppb, due to the low density of data in this range (U.S. EPA, 2013b, section 2.5.4.4). 

Regarding long-term exposures to O3 and mortality changes at lower concentrations, Jerrett et al. 

(2009) evaluated a number of C-R functions with varying threshold levels. Statistical tests 

indicated little discernable improvement in overall model fit when evaluating models that 

included thresholds, however there remained uncertainty about the specific location of the 

threshold, if one did exist (Jerrett et al., 2009; Sasser et al., 2014). In the absence of substantial 

information in the scientific literature on alternative forms of C-R functions at low O3

concentrations, the best estimate of the C-R function is a linear, no-threshold function. The 

scientific literature does not provide sufficient information with which to quantitatively 

characterize any potential additional uncertainty in the C-R functions at lower O3 concentrations 

for use in the quantitative risk assessment. 

Multiple exposures to elevated O3 levels over the course of an O3 season may result in 

adaptation within exposed population. Evidence suggests that repeated or chronic exposures to 

elevated O3 can result in morphologic and biochemical adaptation which reduces the impacts of 

subsequent O3 exposures (U.S. EPA, 2013b, section 6.2.1.1). This has implications for exposure 

modeling, in that the effects of modeled repeat exposures on risk may be attenuated relative to 

the effects of the initial exposures. The ISA notes that “neither tolerance nor attenuation should 

be presumed to imply complete protection from the biological effects of inhaled O3, because 
2-15 

continuing injury still occurs despite the desensitization to some responses (U.S. EPA, 2013b, 

section 6.2.1.1). Because of the complexity of this phenomenon, neither adaptation nor injury 

accumulation resulting from multiple exposures is accounted for in the exposure and associated 

risk modeling performed in Chapters 5 and 6, The ISA reports that there are limited 

epidemiological studies evaluating adaptation to the mortality effects of O3, although the limited 

evidence does suggest that mortality effects are decreased in later months during the O3 season 

relative to earlier months (U.S. EPA, 2013b, section 6.3.3). The impact of this phenomenon on 

risks based on application of results from epidemiological studies is likely to be small, because 

the relative risk estimates from those studies already incorporate any adaptive phenomenon. 

Therefore, adaptation is not explicitly incorporated as an effect modifier in the epidemiologicalbased risk modeling performed in Chapters 7 and 8. 

2.3.4 At-Risk Populations 

The O3 ISA refers to “at-risk” populations as an all-encompassing term used for groups 

with specific factors that increase the risk of an air pollutant- (e.g., O3) related health effect in a 

population group (U.S. EPA, 2013b, chapter 8). Populations or lifestages can experience 

elevated risks from O3 exposure for a number of reasons. These include experiencing high levels 

of exposure due to personal activities that include long durations of time spent in high O3

concentration locations, e.g., outdoor recreation or work, elevated exertion levels that increase 

the dose of O3, e.g., engagement in moderate or strenuous levels of exercise, genetic or other 

biological factors, e.g., lifestage, that may predispose an individual to sensitivity to a given dose 

of O3, pre-existing diseases, e.g., asthma or COPD, and socioeconomic factors that may result in 

more severe health outcomes, e.g., low access to primary care that can lead to increased 

emergency department visits or hospital admissions. To consider risks to these populations, 

modeling of exposures to O3 needs to incorporate information on time spent by potentially at-risk 

populations in high O3 concentration locations. This requires identification of populations with 

the identified exposure-related risk factors, e.g., children or adults engaging in activities 

involving moderate to high levels of outdoor exertion, especially on a repeated basis typical of 

student athletes or outdoor workers, as well as identifying populations with high sensitivity to 

O3, e.g., asthmatic children. It also requires that information on O3 concentrations be mapped to 

locations where at-risk populations are likely to be exposed, e.g., near roadways where running 

may occur, or at schools or parks where children are likely to be engaged in outdoor activities. 

In addition to consideration of factors that lead to increased exposure to O3, modeling of 

risk from O3 exposures should incorporate additional information on factors that can lead to 

increased dose of O3 for a given exposure, e.g., increased breathing rates during periods of 

exertion. These factors are especially important for risk estimates based on application of the 
2-16 

results of controlled human exposure studies. For risk modeling based on application of 

observational epidemiology results, it is also important to understand characteristics of study 

populations that can impact observed relationships between ambient O3 and population health 

responses. 

The O3 ISA identifies a number of factors which have been associated with modifications 

of the effect of ambient O3 on health outcomes. Building on the causal framework used 

throughout the O3 ISA, conclusions are made regarding the strength of evidence for each factor 

that may contribute to increased risk of an O3-related health effect based on the evaluation and 

synthesis of evidence across scientific disciplines. The O3 ISA categorizes potential risk 

modifying factors by the degree of available evidence. These categories include “adequate 

evidence,” “suggestive evidence,” “inadequate evidence,” and “evidence of no effect.” See Table 

8-1 of the O3 ISA for a discussion of these categories (U.S. EPA, 2013b, chapter 8). 

Factors categorized as having adequate evidence include asthma, lifestage (children less 

than 18 years of age, adults older than 65 years of age), diets with nutritional deficiencies, and 

working outdoors. For example, children are the group considered to be at greatest risk because 

they breathe more air per unit of body weight, are more likely to be active outdoors when O3

levels are high, are more likely than adults to have asthma, and are in a critical time period of 

rapid lung growth and organ development. Factors categorized as having suggestive evidence 

include genetic markers, sex (some studies have shown that females are at greater risk of 

mortality from O3 compared to males), low socioeconomic status, and obesity. Factors 

characterized as having inadequate evidence include influenza and other respiratory infections, 

COPD, cardiovascular disease, diabetes, hyperthyroidism, race, and smoking (U.S. EPA, 2013b, 

section 8.5, Table 8-6). 

2.4 URBAN-SCALE MODELING OF INDIVIDUAL EXPOSURE 

Estimates of human exposure to O3 provide important information to inform 

consideration of policy-relevant questions identified in Section 2.2 regarding the occurrence of 

exposures of concern under air quality conditions that meet existing and potential alternative 

standards, and also to provide inputs to the portion of the risk assessment based on application of 

results of controlled human exposure studies. Studies that measure human exposure to O3 are 

limited. More commonly, human exposure is estimated using sophisticated models which 

combine information on ambient O3 concentrations in various microenvironments, e.g., near 

roads, in schools, etc., with information on activity patterns for individuals sampled from the 

general population or specific subpopulations, e.g., children with asthma. 

Ozone exposure is highly dependent on the ambient O3 concentrations in an urban area. 

Given that these concentrations are variable from year to year, it is important to model multiple 
2-17 

years representing the range of variability on O3 concentrations to provide a better 

characterization of potential exposures of concern. In addition, other important sources of 

variability and uncertainty affecting the exposure estimates should be characterized, including 

uncertainty and variability in the data on time-activity patterns, O3 concentrations, and 

population inputs. This can be accomplished in part by modeling exposure for multiple urban 

areas selected to represent variability in these underlying sources of variability. 

This section briefly describes the conceptual foundation for key components of exposure 

modeling, characterization of microenvironmental O3 concentrations, and characterization of 

human activity patterns, including behaviors intended to avert exposures to O3. In addition, a 

brief discussion of key factors to consider in selecting urban study areas for the exposure 

analysis is provided. The specific exposure model used in this assessment, APEX, is described 

more fully in Chapters 3 and 5. Characterization of ambient O3 concentrations is discussed 

earlier in this chapter and in greater detail in Chapter 4. 

2.4.1 Microenvironmental Ozone Concentrations 

Human exposure to O3 involves the contact (via inhalation) between a person and the 

pollutant in the various locations (or microenvironments) in which people spend their time. 

Ozone concentrations in some indoor microenvironments, such as within homes or offices, are 

considerably lower than O3 concentrations in similarly located outdoor microenvironments, 

primarily due to deposition processes and the transformation of O3 into other chemical 

compounds within those indoor microenvironments. Concentrations of O3 may also be quite 

different in roadway environments, such as might occur while an individual is in a vehicle. 

Thus, three important classes of microenvironments that should be considered when 

evaluating population exposures to ambient O3 are indoors, outdoors, and in-vehicle. Within 

each of these broad classes of microenvironments, there are many subcategories, reflecting types 

of buildings, types of vehicles, etc. The O3 ISA evaluated the literature on indoor-outdoor O3

concentration relationships and found that studies consistently show that indoor concentrations 

of O3 are often substantially lower than outdoor concentrations unless indoor sources are present. 

This relationship is greatly affected by the air exchange rate, which can be affected by open 

windows, use of air conditioning, and other factors. Ratios of indoor to outdoor O3

concentrations generally range from about 0.1 to 0.4 (U.S. EPA, 2013b, section 4.3.2). In some 

indoor locations, such as schools, there can be large temporal variability in the indoor-outdoor 

ratios because of differences in air exchange rates over the day. For example, during the school 

day, there is an increase in open doors and windows, so the indoor-outdoor ratio is higher during 

the school day compared with an overall average across all hours and days. In-vehicle 

concentrations are also likely to be lower than ambient concentrations, although the literature 
2-18 

providing quantitative estimates is smaller. Studies of personal exposure to O3 have identified 

that O3 exposures are highest when individuals are in outdoor microenvironments, such as 

walking outdoors midday, moderate when in vehicle microenvironments, and lowest in 

residential indoor microenvironments (U.S. EPA, 2013b, section 4.3.3). Thus the time spent 

indoors, outdoors, and in vehicles is likely to be a critical component in estimating O3 exposures. 

Because of localized chemistry, O3 concentrations on or near roadways can be much 

lower than away from roadways. This is due to the high levels of NOx emissions from motor 

vehicles, which can lead to NOx titration of O3, reducing O3 levels during times of peak traffic. 

The ISA reports evidence that concentrations of NO, NO2, and NOx are negatively correlated 

with concentrations of O3 near busy roadways. Because few monitors are located in direct 

proximity to roadways, it is important to account for differences between near-road O3

concentrations and ambient O3 measurements in modeling exposure. 

2.4.2 Human Activity Patterns 

Human exposure can be measured using several metrics. Exposure to ambient 

concentrations is one such metric. It is also possible to model dose, which combines exposure 

information with physiological parameters related to activity levels. In order to model exposure 

to ambient concentrations, detailed information on the patterns of time spent in different 

microenvironments is critical. In order to model O3 dose, additional information on the activities 

conducted while in those microenvironments is needed, along with data on physiological 

parameters associated with different activities. 

Several large-scale databases of human time-activity-location patterns have been 

compiled. The most comprehensive of these databases in the Consolidated Human Activity 

Database (CHAD), which has been the basis of several previous exposure analyses for previous 

NAAQS reviews. These databases compile large numbers of diaries collected from individual 

study subjects who recorded their time spent performing different activities while in different 

locations, data that were originally collected as part of smaller studies. The ISA notes the high 

degree of variability in activity patterns across the population, as well as the variability in time 

spent in different microenvironments. Time-activity-location patterns vary by age group, as well 

as by region of the U.S. Children generally spend more time in outdoor locations and also 

generally have higher activity levels in those environments. 

The dose of O3 received for any given exposure in a microenvironment depends not only 

on the activity levels and O3 concentrations in the microenvironment, but also on ventilation 

rates, which are related to age, body weight, and other physiological parameters. Children 

generally have lower ventilation rates than adults when considering the volume of air breathed 

per unit time; however, they tend to have a greater oral breathing contribution than adults, and 
2-19 

due to smaller lung volumes and generally greater breathing frequencies, children breathe at 

higher body mass or surface area normalized minute ventilation rates, relative to their lung 

volumes. Both of these factors tend to increase their applied or intake dose normalized to lung 

surface area. For example, when comparing daily body mass normalized ventilation rates, 

children can have up to a factor of two greater ventilation rates when compared to that of adults. 

During periods of high activity, ventilation rates for children and young adults can be nearly 

double those during moderate activity. Thus, it is important to model levels of activity and 

associated ventilation rate as well as time spent in different microenvironments. 

In addition to modeling daily exposures, it may also be important to understand the 

patterns of exposure over an O3 season, including multiple repeated exposures for the same 

individuals. Some individuals or subpopulations may exhibit multiple high daily exposures due 

to persistent patterns of high activity in microenvironments with high O3 concentrations. For 

example, children engaged in numerous outdoor sports over a summer O3 season may have 

multiple exposures to elevated O3 levels. 

Another important issue in characterizing exposure involves consideration of the extent 

to which people in relevant population groups modify their behavior for the purpose of 

decreasing their personal exposure to O3 based on information about predicted air quality levels 

made public through the Air Quality Index (AQI). The AQI is the primary tool EPA has used to 

communicate information on predicted occurrences of high levels of O3 and other pollutants. The 

AQI provides both the predicted level of air quality in an area along with a set of potential 

actions that individuals and communities can take to reduce exposure to air pollution and thus 

reduce the risk of health effects associated with breathing ambient air pollution. There are 

several studies, discussed in the O3 ISA, that have evaluated the degree to which populations are 

aware of the AQI and what actions individuals and communities take in response to AQI values 

in the unhealthy range. These studies suggest that at-risk populations, such as children, older 

adults, and asthmatics, modify their behavior in response to days with bad air quality, most 

commonly by reducing their time spent outdoors or limiting their outdoor activity exertion level. 

A challenge remains in how to consider existing averting behaviors within the assessment tools 

we use and how best to use improved knowledge of participation rates, the varying types of 

actions performed particularly by potentially at-risk individuals, and the duration of these 

averting behaviors to quantify the impact on estimated exposures and health risks. 

2.4.3 Modeling of Exposures Associated with Simulating Just Meeting Ozone Standards 

In order to address policy-relevant questions regarding changes in exposure associated 

with potential alternative standards, the exposure assessment evaluates changes in the O3

concentrations, and the resulting changes in exposure, associated with simulating just meeting 
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alternative standards relative to just meeting the existing standards. The new, model-adjustment 

methodology being implemented in this risk and exposure assessment provides for more realistic 

responses of hourly O3 concentrations to changes in the precursor emissions that lead to O3

formation. Characterization of exposure and changes in exposure when simulating just meeting 

the alternative standards are discussed in greater detail in Chapter 5. 

2.4.4 Considerations in Selecting Urban Study Areas for the Exposure Analysis 

The goal of the urban-scale exposure analysis is to characterize the variability in 

exposures for different geographic locations, taking into account variability in essential factors 

that affect exposures. Important factors identified earlier that may influence exposure include 

time activity patterns, especially activities occurring in outdoor environments; demographics of 

the exposed population, e.g., age and income level; and O3 concentrations. In addition to these 

factors, the selection of urban areas to include in the exposure analysis takes into consideration 

the location of O3 epidemiological studies (for comparability with the risk assessments), the 

availability of ambient O3 data and specific exposure information (e.g., air conditioning 

prevalence), and the desire to represent a range of geographic areas. To make the exposure 

analysis most useful in addressing the key policy-relevant questions, urban study areas were also 

chosen such that most of them exceeded the existing 8-hr O3 standards and potential alternative 

standards during the time period of interest. 

2.5 URBAN- AND NATIONAL-SCALE RISK ASSESSMENT 

Assessment of risk entails joint consideration of the exposure to a hazard, frequency of 

adverse outcomes given exposure, and severity of resulting adverse outcomes. A risk assessment 

for O3 requires characterization of exposures to ambient O3 for relevant populations, 

identification of appropriate dose-response or C-R functions linking O3 with adverse health 

outcomes, and characterizing risks for individuals and populations. 

As discussed above, there are two classes of studies that have provided information to 

inform the risk modeling: controlled human exposure studies and observational epidemiology 

studies. The conceptual approach to risk assessment varies based on which type of study result is 

being applied. This section briefly describes the conceptual foundation for several aspects of risk 

modeling, including the concept of attributable risk, modeling of total risk and incremental risk 

reductions, development of risk estimates based on controlled human exposure studies, and 

development of risk estimates based on results of observational epidemiology studies. 

This section briefly describes the conceptual foundation for key elements of risk 

modeling, including a discussion of the concept of attributable risk, modeling of risk for total O3

exposure and the distribution of risk over O3 concentrations, modeling of risk reductions 
2-21 

associated with alternative standards, and key factors to consider in selecting urban study areas 

for the risk analysis. Characterization of ambient O3 concentrations is discussed earlier in this 

chapter and in greater detail in Chapter 4. The specific risk models used in the urban-scale risk 

analyses, APEX for analyses based on application of controlled human exposure studies and 

BenMAP for analyses based on application of observational epidemiology studies, are described 

more fully in Chapters 6 and 7, respectively. Chapter 8 provides an additional national-scale 

assessment of mortality risk associated with recent O3 concentrations, to provide context for 

evaluating the magnitude of health risks in the urban study areas and to evaluate the 

representativeness of the urban study areas in estimating O3 risks. 

2.5.1 Attributable Risk 

This risk and exposure assessment relies on the concept of attributable risk in evaluating 

both total risk and incremental changes in risk associated with just meeting existing and potential 

alternative O3 standards. Attributable risk is defined as the difference in incidence of an adverse 

effect between an exposed and unexposed population for a specific stressor. Attributable risk is 

an important concept when addressing risks that are associated with multiple causes, such as 

mortality and respiratory hospital admissions. 

Estimates of attributable risk require either an E-R function (for analyses based on results 

of controlled human exposure studies) or a C-R function (for analyses based on results of 

epidemiology studies). 

E-R functions require estimates of exposure to calculate health risk, and in this case 

exposures are supplied by the APEX modeling described above. In the case of the lung function 

endpoint evaluated in this risk analysis, the E-R function also requires information on age and 

exertion levels to predict the impact of O3 exposure on decrements in lung function. E-R 

functions may provide estimates of the incidence of an endpoint or the probability of exceeding 

benchmark decrement levels. 

C-R functions derived from relative risk estimates reported in the epidemiological 

literature generally require estimates of ambient O3 concentrations, baseline incidence rates, and 

estimates of exposed populations to calculate health risk. Ambient O3 concentrations should 

generally be constructed to match the spatial and temporal averaging used in the underlying 

epidemiology study; e.g., a study may have used a spatial average over a metropolitan statistical 

area of the daily maximum 8-houraverage concentration. 

As with exposure, attributable risk is highly dependent on the ambient O3 concentrations 

in an urban area. Given that these concentrations are variable from year to year, it is important to 

model multiple years representing the range of variability of O3 concentrations to provide a 

better characterization of risk. In addition, other important sources of variability and uncertainty 
2-22 

affecting the risk estimates should be characterized, including uncertainty and variability in the 

C-R and E-R functions, O3 concentrations and O3 exposure, and population inputs. This can be 

accomplished in part by modeling risk for multiple urban areas selected to represent variability in 

these underlying risk drivers. 

2.5.2 Modeling of Health Risk Associated with Total Ozone Exposure 

 As discussed earlier in this chapter, ambient O3 is contributed to by emissions from a 

variety of sources, including natural, U.S. anthropogenic, and non-U.S. anthropogenic sources. 

Once in the atmosphere, O3 molecules created from these different sources of emissions are not 

distinguishable. Individuals and populations are exposed to total O3 from all sources, and risks 

associated with O3 exposure are due to total O3 exposure and do not vary for O3 exposure 

associated with any specific source including background sources, regardless of how they may 

be defined. Given the absence of a detectable threshold in the available C-R functions, total risk 

attributable to O3 will thus be the risk associated with total exposure to O3, with no threshold or 

cut-point applied. To address certain policy-related questions, it is possible to approximately 

attribute risk to specific sources through the use of air quality modeling techniques, and this is 

explored in the PA. However, these techniques are based on applying model results to total O3

risk, rather than on directly modeling risk attributable to specific sources. 

As discussed earlier in this chapter, a critical policy-relevant risk question is the O3

attributable risk remaining after just meeting the existing O3 standards. This risk includes risks 

associated with O3 from all sources after we have simulated just meeting the existing daily 

maximum 8-hour standard level of 75 ppb. The estimates of total risk remaining after meeting 

the existing standard form the reference values for evaluating reductions in risk associated with 

just meeting alternative levels of the standard. 

In addition to providing risk estimates for urban study areas, it is also useful to evaluate 

O3 risks across the entire U.S., both to better understand the total magnitude of the health burden 

associated with O3 exposures and to evaluate the representativeness of selected urban study areas 

in characterizing the range and variability in risks across the U.S. The national-scale risk 

assessment presented in Chapter 8 is focused on estimating risk associated with recent O3

concentrations, rather than on risk after just meeting existing or alternative standards. This is the 

appropriate focus for the national-scale analysis, because the techniques used to simulate just 

meeting existing and alternative standards in urban study areas are less certain in a national 

context due to concerns about interdependence between air quality responses in different urban 

areas; e.g., just meeting a standard in one urban area would likely have impacts on O3 air quality 

in surrounding urban areas. It is beyond the scope of this HREA to simulate a full suite of all 
2-23 

possible control strategies that would result in just meeting existing or alternative primary health 

standards. 

2.5.3 Distributions of Risk Across Ozone Concentrations 

Total O3 risk for the O3 season is calculated by summing daily risks across all days in the 

O3 season. Because of the high degree of variability in daily O3 concentrations across an O3

season, total O3 risk will include risks calculated for some days with high O3 concentrations as 

well as for some days with very low O3 concentrations. Therefore it is appropriate to provide the 

distribution of total risk over the range of daily O3 concentrations to allow for an understanding 

of how O3 concentrations on different days are contributing to the estimates of total risk. In 

addition, as noted in the ISA and discussed above, because C-R functions are commonly 

comprised of fewer days with low O3 concentrations of compared with the number of high 

concentration days, there is decreased confidence in the shape of the C-R function at lower O3

concentrations, and therefore lower confidence in risk estimates for days with lower O3

concentrations, especially in the range below 20 ppb. As a result, it is appropriate to provide the 

distribution of total risk over the range of daily O3 concentrations to allow for better 

characterization of confidence in the estimates of total risk. 

2.5.4 Modeling Risk Associated with Simulating Just Meeting Ozone Standards 

In order to address policy-relevant questions regarding changes in risk associated with 

potential alternative standards, the risk assessment evaluates changes in the distribution of O3

concentrations, and the resulting changes in risk, associated with simulating just meeting 

alternative standards relative to just meeting the existing standards. The new, model-adjustment 

methodology being implemented in this risk and exposure assessment provides for more realistic 

responses of hourly O3 concentrations to changes in the precursor emissions that lead to O3

formation than when compared with that using a purely statistical-based approach.8 As noted 

earlier there are multiple combinations of reductions in precursor emissions that can result in just 

meeting alternative standards. As a result, there is variability in the potential changes in the 

distribution of O3 concentrations and risk that would result from just meeting existing and 

alternative standards. Characterization of this variability, as well as uncertainties in the 

simulation of just meeting the standards, will be included in Chapters 6 and 7. 

 

8

 The new, model-adjustment approach captures the nonlinearity of O3 response to emissions changes, representing 

both increases and decreases in O3 concentrations resulting from emissions reductions. In addition, HDDM 

characterizes different O3 response at different locations (downtown urban versus downwind suburban) and at 

different times of day allowing us to incorporate temporal and spatial variations in response into the O3 adjustment 

methodology. Finally, HDDM eliminates the need to use background O3 as a floor for adjustment because 

predicted sensitivities are based on model formulations that explicitly account for background sources. 
2-24 

2.5.5 Considerations in Selecting Urban Study Areas for the Risk Assessment 

The goal of the urban-scale risk analysis is to characterize the magnitude of risk and the 

impact on risk of meeting existing and potential alternative standards. The selection of specific 

urban study areas is based on a set of factors reflecting both variability in factors that affect risk 

and availability of high quality input data, to provide risk estimates that have higher overall 

confidence. Important factors identified earlier that may influence risk include O3 concentrations, 

demographics, exposure factors, and magnitude of the effect estimate in the C-R function. In 

addition to consideration of variability in these factors, urban study areas are preferentially 

selected if they have O3 concentrations that are above the existing standards and potential 

alternative standards, if they have suitable epidemiological studies to provide C-R functions for 

mortality or morbidity, if they have adequate monitoring data available to characterize 

population exposures, and if they have appropriate baseline health incidence data available. 

2.6 RISK CHARACTERIZATION 

Risk characterization is the process of communicating the results of risk (and exposure) 

modeling in metrics that have meaning to decision-makers. In the specific context of this review, 

this translates into providing metrics that are most useful in the O3 PA to assess the adequacy of 

the existing O3 standards in protecting public health with an adequate margin of safety and to 

evaluate the additional protection provided by potential alternative standards. 

Risk characterization requires careful translation of very complex outputs of exposure 

and risk models into simpler metrics, for example, translating hourly O3 exposures in various 

microenvironments into estimates of population exposures above alternative exposure 

benchmarks. Risk characterization also requires the condensation of a large number of analytical 

steps and results to (a) summarize the results of the risk analysis, usually taking detailed results 

and condensing them into a more aggregate interpretation while still providing information about 

heterogeneity across space and time; (b) communicate the sensitivity of results to different 

modeling assumptions; and (c) characterize the qualitative and quantitative uncertainty in results. 

As described more fully in Chapter 5 and in the O3 PA, EPA has selected, based on 

providing a reasonable measure of exposures of concern for at-risk populations and lifestages, 

aggregate exposure metrics including the number and percent of certain highly vulnerable 

populations exposed to levels of O3 above exposure levels that have been identified in the 

scientific literature as associated with adverse respiratory responses (i.e., pulmonary function 

decrements and increases in respiratory symptoms, lung inflammation, lung permeability, and airway 

hyper-responsiveness). As noted in section 2.3.1 above, these benchmark exposure levels are 

0.060 ppm, 0.070 ppm, and 0.080 ppm. Important at-risk populations include active children, 

older adults, and outdoor workers. 
2-25 

As described more fully in Chapters 6 and 7 and in the O3 PA, EPA has selected, based 

on providing characterization of risks to the public including at-risk populations and lifestages, 

aggregate risk metrics including the number and percent of vulnerable populations experiencing 

adverse respiratory responses based on application of results of controlled human exposure 

studies and the attributable incidence and percent of baseline incidence of mortality and 

morbidity endpoints based on application of results of epidemiology studies. 

For all three types of metrics (exposure, risk based on controlled human exposure studies, 

and risk based on epidemiology studies) and for the purpose of evaluating the adequacy of the 

existing standards, the focus is on the exposure and risk remaining upon just meeting the existing 

standards. For the purpose of evaluating alternative standards, the focus in on the changes in 

exposure and risk after simulating just meeting the alternative standards, compared to exposures 

and risk after simulating just meeting the existing standards. 

As detailed in Chapter 3, quantitative sensitivity analyses are provided to evaluate the 

impacts of critical inputs to the exposure and risk modeling. Limited quantitative uncertainty 

analyses are also included, along with a comprehensive qualitative uncertainty assessment. The 

overall treatment of uncertainty is guided by the World Health Organization (WHO) guidelines 

for uncertainty assessment (WHO, 2008). These guidelines recommend a tiered approach in 

which progressively more sophisticated methods are used to evaluate and characterize sources of 

uncertainty depending on the overall complexity of the risk assessment. 

In order to inform considerations of overall confidence in the risk estimates derived from 

application of C-R functions derived from the epidemiological literature, we provide the 

distributions of total risk across the entire range of daily maximum 8-hour O3 concentrations. In 

addition, we provide an assessment of the representativeness of the urban study areas selected for 

the risk and exposure analysis in characterizing the overall distribution of risk across the U.S. 

This assessment evaluates how well the selected urban study areas capture important 

characteristics that are associated with risk, including demographics, air quality levels, and 

factors affecting exposure such as air conditioning prevalence.
2-26 

2.7 REFERENCES 

Frey, C. and J. Samet. 2012. CASAC Review of the EPA’s Policy Assessment for the Review of 

the Ozone National Ambient Air Quality Standards (First External Review Draft – 

August 2012). U.S. Environmental Protection Agency Science Advisory Board. EPACASAC-13-003. 

Jaegle, L.; D.J. Jacob; W.H. Brune; and P.O. Wennberg. 2001. Chemistry of HOx radicals in the 

upper troposphere. Atmos Environ. 35:469-489. 

Jerrett, M.; R.T. Burnett; C.A. Pope, III; K. Ito; G. Thurston; D. Krewski; Y. Shi; E. Calle; and 

M. Thun. 2009. Long-term O3 exposure and mortality. NEJM. 360:1085-1095. 

NRC. 2009. Science and Decisions: Advancing Risk Assessment. National Research Council, 

Washington, DC: The National Academies Press. 

Sasser, E. 2014. Response to Comments Regarding the Potential Use of a Threshold Model in 

Estimating the Mortality Risks from Long-term Exposure to Ozone in the Health Risk 

and Exposure Assessment for Ozone, Second External Review Draft. Memorandum to 

Holly Stallworth, Designated Federal Officer, Clean Air Scientific Advisory Committee 

from EPA/OAQPS Health and Environmental Impacts Division. 

U.S. EPA. 2011. Integrated Review Plan for the O3 National Ambient Air Quality Standards. 

Research Triangle Park, NC: National Center for Environmental Assessment, Office of 

Research and Development and Office of Air Quality Planning and Standards, Office of 

Air and Radiation. (EPA document number EPA 452/R-11-006). 

<http://www.epa.gov/ttn/naaqs/standards/ozone/data/2011_04_OzoneIRP.pdf>. 

U.S. EPA. 2012a. Total Risk Integrated Methodology (TRIM) - Air Pollutants Exposure Model 

Documentation (TRIM.Expo / APEX, Version 4.4) Volume I: User’s Guide. Research 

Triangle Park, NC: EPA Office of Air Quality Planning and Standards. (EPA document 

number EPA-452/B-12-001a). <http://www.epa.gov/ttn/fera/human_apex.html>. 

U.S. EPA. 2012b. Total Risk Integrated Methodology (TRIM) - Air Pollutants Exposure Model 

Documentation (TRIM.Expo / APEX, Version 4.4) Volume II: Technical Support 

Document. Research Triangle Park, NC: Office of Air Quality Planning and Standards. 

(EPA document number EPA-452/B-12-001b). 

< http://www.epa.gov/ttn/fera/human_apex.html>. 

U.S. EPA. 2013a. Environmental Benefits Mapping Analysis Program (BenMAP v4.0). Posted 

January, 2013. < http://www.epa.gov/air/benmap/download.html />. 

U.S. EPA. 2013b. Integrated Science Assessment of Ozone and Related Photochemical Oxidants 

(Final Report). Research Triangle Park, NC: EPA Office of Research and Development. 

(EPA document number EPA/600/R-10/076F). 

<http://cfpub.epa.gov/ncea/isa/recordisplay.cfm?deid=247492#Download>. 

WHO. 2008. Part 1: Guidance Document on Characterizing and Communicating Uncertainty in 

Exposure Assessment, Harmonization Project Document No. 6. Published under joint 

sponsorship of the World Health Organization (WHO), the International Labor 

Organization and the United Nations Environment Programme. WHO Press, World 

Health Organization, 20 Avenue Appia, 1211 Geneva 27, Switzerland. 
3-1

3 SCOPE 

This chapter provides an overview of the scope and key design elements of this 

quantitative exposure and health risk assessment. The design of this assessment began with a 

review of the exposure and risk assessments completed during the last O3 NAAQS review (U.S. 

EPA, 2007a,b), with an emphasis on considering key limitations and sources of uncertainty 

recognized in that analysis. 

As an initial step in the current O3 NAAQS review in October 2009, EPA invited outside 

experts, representing a broad range of expertise (e.g., epidemiology, human and animal 

toxicology, statistics, risk/exposure analysis, atmospheric science), to participate in a workshop 

with EPA staff to help inform EPA’s plan for the review. The participants discussed key policyrelevant issues that would frame the review and the most relevant new science that would be 

available to inform our understanding of these issues. One workshop session focused on planning 

for quantitative risk and exposure assessments, taking into consideration what new research 

and/or improved methodologies would be available to inform the design of quantitative exposure 

and health risk assessment. Based in part on the workshop discussions, EPA developed a draft 

IRP (U.S. EPA, 2009a) outlining the schedule, process, and key policy-relevant questions that 

would frame this review. On November 13, 2009, EPA held a consultation with CASAC on the 

draft IRP (74 FR 54562, October 22, 2009), which included opportunity for public comment. 

The final IRP incorporated comments from CASAC (Samet, 2009) and the public on the draft 

plan, as well as input from senior Agency managers. The final IRP included initial plans for 

quantitative risk and exposure assessments for both human health and welfare (U.S. EPA, 2011a, 

chapters 5 and 6). 

As a next step in the design of these quantitative assessments, OAQPS staff developed 

more detailed planning documents, the Ozone National Ambient Air Quality Standards: Scope 

and Methods Plan for Health Risk and Exposure Assessment (Health Scope and Methods Plan, 

U.S. EPA, 2011b) and the Ozone National Ambient Air Quality Standards: Scope and Methods 

Plan for Welfare Risk and Exposure Assessment (Welfare Scope and Methods Plan, U.S. EPA, 

2011c). These Scope and Methods Plans were the subject of a consultation with CASAC on May 

19-20, 2011 (76 FR 23809, April 28, 2011). Based on consideration of CASAC (Samet, 2011) 

and public comments on the Scope and Methods Plans, and information in the second draft ISA, 

we modified the scope and design of the quantitative risk assessment and provided a memo with 

updates to information presented in the Scope and Methods Plans (Wegman, 2012). The Scope 

and Methods Plans together with the update memo provide the basis for the discussion of the 

scope of this exposure and risk assessment provided in this chapter. This chapter also reflects 
3-2

comments received from CASAC based on their review of the draft Risk and Exposure 

Assessments (Frey and Samet, 2012a; Frey, 2014). 

In presenting the scope and key design elements of the current risk assessment, this 

chapter first provides a brief overview of the quantitative exposure and risk assessment 

completed for the previous O3 NAAQS review in section 3.1, including key limitations and 

uncertainties associated with that analysis. The remaining sections describe the current exposure 

and risk assessment, following the general conceptual framework described in Chapter 2. Section 

3.2 provides a summary of the design of the urban-scale exposure assessment. Section 3.3 

provides a summary of the design of the urban-scale risk assessment based on application of 

results of human clinical studies. Section 3.4 provides a summary of the design of the urbanscale risk assessment based on application of results of epidemiology studies. Section 3.5 

provides a summary of the design of the national-scale risk burden assessment and 

representativeness analysis. 

3.1 OVERVIEW OF THE EXPOSURE AND RISK ASSESSMENTS FROM THE 

LAST REVIEW 

The exposure and health risk assessment conducted in the review, completed in March 

2008, developed exposure and health risk estimates for 12 urban areas across the U.S. which 

were chosen based on the location of O3 epidemiological studies and availability of ambient O3

data and to represent a range of geographic areas, population demographics, and O3 climatology. 

That analysis was in part based upon the exposure and health risk assessments included in the 

review completed in 1997.1

The exposure and risk assessment incorporated air quality data (i.e., 

2002 through 2004), and provided annual or O3 season-specific exposure and risk estimates for 

these recent years of air quality and for air quality scenarios simulating just meeting the existing 

8-hour (8-hr) O3 standard and several alternative 8-hr O3 standards. 

3.1.1 Overview of Exposure Assessment from the Last Review 

Exposure estimates were used as an input to the risk assessment for lung function 

responses (a health endpoint for which exposure-response (E-R) functions were available from 

controlled human exposure studies). Exposure estimates were developed for the general 

population and study groups including asthmatic school-age children (ages 5-18) as well as all 

 

1

 In the 1994-1997 O3 NAAQS review, EPA conducted exposure analyses for the general population, children who 

spent more time outdoors, and outdoor workers. Exposure estimates were generated for 9 urban areas for base air 

quality and for air quality adjusted to just meeting the then-existing 1-hr standard and several alternative 8-hr 

standards. Several reports that describe these analyses can be found at: 

http://www.epa.gov/ttn/naaqs/standards/ozone3/s_o3_pr.html. 
3-3

school-age children. The exposure estimates also provided information on population exposures 

exceeding potential health effect benchmark levels that were identified based on the observed 

occurrence of health endpoints not explicitly modeled in the health risk assessment (e.g., lung 

inflammation, increased airway responsiveness, and decreased resistance to infection) associated 

with 6- to 8-hr exposures to O3 in controlled human exposure studies. 

The exposure analysis took into account several important factors including the 

magnitude and duration of exposures, frequency of repeated high exposures, and breathing rate 

of individuals at the time of exposure. Estimates were developed for several indicators of 

exposure to various levels of O3 air quality, including counts of people exposed one or more 

times to a given O3 concentration while at a specified breathing rate and counts of personoccurrences (which accumulate occurrences of specific exposure conditions over all people in 

the population groups of interest over an O3 season). 

As discussed in the O3 exposure assessment (U.S. EPA, 2007a), a technical support 

document (Langstaff, 2007), the 2007 Staff Paper (U.S. EPA, 2007c) and in Section II a of the 

O3 Final Rule (73 FR 16440 to 16442, March 27, 2008), the most important uncertainties 

affecting the exposure estimates were related to modeling human activity patterns over an O3

season, modeling of variations in ambient concentrations near roadways, and modeling of air 

exchange rates that affect the amount of O3 that penetrates indoors. Another important 

uncertainty, discussed in more detail in the Staff Paper (U.S. EPA, 2007c, section 4.3.4.7), was 

the uncertainty in energy expenditure values which directly affected the modeled breathing rates. 

These were important because they were used to classify exposures occurring when children 

were engaged in moderate or greater exertion. Health effects observed in the controlled human 

exposure studies generally occurred under these exertion levels for 6 to 8-hr exposures to O3

concentrations at or near 0.08 ppm. 

3.1.2 Overview of Risk Assessment from the Last Review 

The human health risk assessment presented in the review completed in March 2008 was 

designed to estimate population risks in a number of urban areas across the U.S., consistent with 

the scope of the exposure analysis described above (U.S. EPA, 2007a,b,c). The risk assessment 

included risk estimates based on both controlled human exposure studies and epidemiological 

and field studies. O3-related risk estimates for lung function decrements were generated using 

probabilistic E-R relationships based on data from controlled human exposure studies, together 

with population-based probabilistic exposure estimates from the exposure analysis. For several 

other health endpoints, O3-related risk estimates were generated using concentration-response 

(C-R) relationships reported in epidemiological or field studies, together with ambient air quality 

concentrations, baseline health incidence rates, and population data for the various locations 
3-4

included in the assessment. Health endpoints included in the assessment based on 

epidemiological or field studies included hospital admissions for respiratory illness in four urban 

areas, premature mortality in 12 urban areas, and respiratory symptoms in asthmatic children in 1 

urban area. 

In the health risk assessment conducted in the previous review, EPA recognized that there 

were many sources of uncertainty and variability in the inputs to the assessment and that there 

was significant uncertainty in the resulting risk estimates. The statistical uncertainty surrounding 

the estimated O3 coefficients in epidemiological-based C-R functions as well as the shape of the 

E-R relationship chosen for the lung function risk assessment were addressed quantitatively. 

Additional uncertainties were addressed through sensitivity analyses and/or qualitatively. The 

risk assessment conducted for the previous O3 NAAQS review incorporated some of the 

variability in key inputs to the assessment by using location-specific inputs (e.g., locationspecific C-R functions, baseline incidence rates and population data, and air quality data for 

epidemiological-based endpoints, location specific air quality data and exposure estimates for the 

lung function risk assessment). In that review, several urban areas were included in the health 

risk assessment to provide some insight as to variability in the risk estimates across the U.S. 

Key observations and insights from the O3 risk assessment, in addition to important 

caveats and limitations, were addressed in Section II.B of the Final Rule notice (73 FR 16440 to 

14 16443, March 27, 2008). In general, estimated risk reductions associated with going from 

then-current O3 levels to just meeting the then-existing and alternative 8-hr standards showed 

patterns of decreasing estimated risk associated with just meeting the lower alternative 8-hr 

standards considered. Furthermore, the estimated percentage reductions in risk were strongly 

influenced by the baseline air quality year used in the analysis, which was due to significant 

year-to-year variability in O3 concentrations. There was also noticeable city-to-city variability in 

the estimated O3-related incidence of morbidity and mortality across the 12 urban areas. 

Uncertainties associated with estimated policy-relevant background (PRB) concentrations2 were 

also addressed and revealed differential impacts on the risk estimates depending on the health 

effect considered as well as the location. EPA also acknowledged that at the time of the previous 

review there were considerable uncertainties surrounding estimates of O3 C-R coefficients and 

the shape of C-R relationships and whether or not a population threshold or non-linear 

relationship exists within the range of concentrations examined in the epidemiological studies. 

 

2

 Policy-relevant background (PRB) O3 has been defined in previous reviews as the distribution of O3 concentrations 

that would be observed in the U.S. in the absence of anthropogenic (man-made) emissions of O3 precursor 

emissions (e.g., VOC, CO, NOx) in the U.S., Canada, and Mexico. 
3-5

3.2 PLAN FOR THE CURRENT EXPOSURE AND RISK ASSESSMENTS 

The Scope and Methods Plan, including updates (U.S. EPA, 2011b; Wegman, 2012), 

outlined a planned approach for conducting the current quantitative O3 exposure and risk 

assessments, including broad design issues as well as more detailed aspects of the analyses. A 

critical step in designing the quantitative risk and exposure assessments is to clearly identify the 

goals for the analysis based on the policy-relevant questions identified in Chapter 2. We have 

identified the following goals for the urban area exposure and risk assessments: (1) to provide 

estimates of the percent and number of people in the general population and in sensitive 

populations with O3 exposures above health-based benchmark levels; (2) to provide estimates of 

the percent and number of the general population and in sensitive populations with impaired lung 

function (defined based on decrements in FEV1) resulting from exposures to O3; (3) to provide 

estimates of the potential magnitude of premature mortality associated with both short-term and 

long-term O3 exposures, and selected morbidity health effects associated with short-term O3

exposures; (4) to evaluate the influence of various inputs and assumptions on exposure and risk 

estimates to the extent possible given available methods and data; (5) to gain insights into the 

spatial and temporal distribution of risks and patterns of risk reduction and uncertainties in those 

risk estimates. For the exposure and risk analyses, we will estimate exposures and risks for 

recent (2006 – 2010) ambient levels of O3 and for O3 concentrations after simulating just 

meeting the existing O3 standard and potential alternative standards. 

With regard to selecting alternative levels for the 8-hr O3 standards for evaluation in the 

quantitative risk assessment, we base the range of levels on the evaluations of the evidence 

provided in the PA, which received support from the CASAC in their advisory letter (Frey and 

Samet, 2012b). The PA recommended evaluation of daily maximum 8-hr average concentrations 

in the range of 60 to 70 ppb, with possible consideration of levels somewhat below 60 ppb. The 

upper end of this range is supported by the clear evidence from both clinical and epidemiological 

studies of effects at exposures of 70 ppb reported in the ISA and summarized in the PA. The 

lower end of this range is based on considerations of evidence from clinical studies that have 

shown lung function decrements in healthy adult populations at 60 ppb O3 exposures, and that 10 

percent of healthy adults exposed to 60 ppb O3 experienced lung function decrements that could 

be adverse to asthmatics. The evidence showing effects in healthy adults at exposures of 60 ppb 

supports the consideration of risks to sensitive populations at exposure levels below 60 ppb, 

although specific exposure levels below 60 ppb at which risks may be occurring are not 

supported by the evidence. An important distinction is that the evidence from controlled human 

exposure studies is based on actual exposure concentrations, while the standard is set to address 

ambient concentrations. Typically, exposures are lower than ambient concentrations because 
3-6

people tend to spend a large fraction of their time indoors where O3 concentrations are 

substantially lower.3

Because of the year-to-year variability in O3 concentrations that results from temporal 

variability in meteorology and emissions that drive O3 formation, the exposure and risk 

assessments evaluate scenarios for meeting the existing and alternative standards based on 

multiple years of O3 data. Ozone concentrations from 2006-2010 are used in estimating exposure 

and risk. This range of years captures a high degree of variability in meteorological conditions, 

as well as reflecting years with higher and lower emissions of O3 precursors. 

In order to provide greater confidence in the exposure and risk estimates, this health REA 

(HREA) uses an urban-scale analysis approach for assessing both exposure and risk. This 

approach provides greater confidence in estimates by allowing us to make use of air quality data, 

population information, health data, and epidemiology results that are well matched, and it does 

not require extrapolation of results to areas without these data. In addition, the urban-scale 

analysis approach allows us to simulate just meeting existing and alternative O3 standards for 

each urban study area, which is not currently feasible for health risk assessment at the nationalscale.4

 Specific selection criteria for urban study areas included in the exposure and risk 

assessments are described in the following sections. In order to gain an understanding of how 

well the urban study areas represent risks at a national level and to provide context for the urbanscale analysis results, we also include two national-scale analyses, (1) estimation of the nationalscale mortality burden associated with recent (2007) ambient O3 and (2) characterization of how 

well the risk estimates for the set of urban areas modeled reflect the national-scale distribution of 

mortality risk. 

Throughout the exposure and risk analyses, we recognize that there are many sources of 

variability and uncertainty. Each analysis considers carefully the potential sources and 

significance of variability and uncertainties and, where data are available, provides quantitative 

assessment of variability and uncertainties, either through probabilistic analyses or through 

sensitivity or scenario analyses. In general the analyses follow the World Health Organization 

(WHO) guidelines for uncertainty assessment (WHO, 2008), which recommend a tiered 

 

3

 While almost all people spend a large fraction of their time indoors, there is high variability in this fraction 

between children and adults, and between outdoor workers and indoor workers. The ratio of exposures to ambient 

concentrations will likely be higher for children than adults, and for outdoor workers compared to indoor workers. 4

 In order to simulate just meeting alternative standards everywhere nationwide using the model-based adjustment 

approach employed in this HREA, some areas would see O3 design values decreased below the targeted standard 

level due to O3 transport between locations. We were not able to devise an approach that would just meet the 

standard in every location simultaneously. Using the urban-scale analysis approach, we can, acknowledging the 

counterfactual nature of the analysis, assume independence of each urban study area, which allows us to simulate 

just meeting the standards in each urban study area. 
3-7

approach in which progressively more sophisticated methods can be used to evaluate and 

characterize sources of uncertainty depending on the overall complexity, end use of the 

assessment, and resources and data available to conduct particular uncertainty characterizations. 

The planned approaches for conducting the exposure and risk analyses are briefly 

summarized below. We begin with a general discussion of how uncertainty and variability are 

addressed in the different elements of the exposure and risk assessment. This is followed by a 

discussion of the air quality data that will be used in both the exposure and risk assessments and 

then discussions of each component of the exposure and risk assessments. 

3.3 CHARACTTERIZATION OF UNCERTAINTY AND VARIABILITY IN THE 

CONTEXT OF THE OZONE EXPOSURE AND RISK ASSESSMENT 

An important component of this population exposure and health risk assessment is the 

characterization of both uncertainty and variability. Variability refers to the heterogeneity of a 

variable of interest within a population or across different populations. For example, populations 

in different regions of the country may have different behavior and activity patterns (e.g., air 

conditioning use and time spent indoors) that affect their exposure to ambient O3 and thus the 

population health response. The composition of populations in different regions of the country 

may vary in ways that can affect the population response to exposure to O3 – e.g., two 

populations exposed to the same levels of O3 might respond differently if one population has a 

greater proportion of older people than the other. Variability is inherent and cannot be reduced 

through further research. Refinements in the design of a population risk assessment are often 

focused on more completely characterizing variability in key factors affecting population risk – 

e.g., factors affecting population exposure or response – to produce risk estimates whose 

distribution adequately characterizes the distribution in the underlying population(s). 

Uncertainty refers to the lack of knowledge regarding the actual values of inputs to an 

analysis. Models are typically used in analyses, and there is uncertainty about the true values of 

the model inputs and their parameterization (parameter uncertainty) – e.g., the value of the 

coefficient for O3 in a C-R function. There is also uncertainty about the extent to which the 

model is an accurate representation of the underlying physical systems or relationships being 

modeled (model uncertainty) – e.g., the shapes of C-R functions. In addition, there may be some 

uncertainty surrounding other inputs to an analysis due to possible measurement error – e.g., the 

values of daily O3 concentrations in a risk assessment location or the value of the baseline 

incidence rate for a health effect in a population.5

 

5

 It is also important to point out that failure to characterize variability in an input used in modeling can also 

introduce uncertainty into the analysis. This reflects the important link between uncertainty and variability with 
3-8

In any risk assessment, uncertainty is, ideally, reduced to the maximum extent possible 

through improved measurement of key variables and ongoing model refinement. However, 

significant uncertainty often remains, and emphasis is then placed on characterizing the nature of 

that uncertainty and its impact on risk estimates. The characterization of uncertainty can be both 

qualitative and, if a sufficient knowledge base is available, quantitative. 

The characterization of uncertainty associated with risk assessment is ideally addressed in 

the regulatory context using a tiered approach in which progressively more sophisticated 

methods are used to evaluate and characterize sources of uncertainty depending on the overall 

complexity and intended use of the risk assessment (WHO, 2008). Guidance documents 

developed by EPA for assessing air toxics-related risk and Superfund Site risks as well as recent 

guidance from WHO specify multitier approaches for addressing uncertainty. 

Following the approach used for previous NAAQS risk and exposure assessments (U.S. 

EPA, 2008, 2009b, 2010a, b), for the O3 risk assessment, we are using a tiered framework 

developed by WHO to guide the characterization of uncertainty. The WHO guidance presents a 

four-tiered approach, where the decision to proceed to the next tier is based on the outcome of 

the previous tier’s assessment. The four tiers described in the WHO guidance include: 

 Tier 0: recommended for routine screening assessments, uses default uncertainty factors 

(rather than developing site-specific uncertainty characterizations); 

 Tier 1: the lowest level of site-specific uncertainty characterization, involves qualitative 

characterization of sources of uncertainty (e.g., a qualitative assessment of the general 

magnitude and direction of the effect on risk results); 

 Tier 2: site-specific deterministic quantitative analysis involving sensitivity analysis, 

interval-based assessment, and possibly probability bounded (high-and low-end) 

assessment; and 

 Tier 3: uses probabilistic methods to characterize the effects on risk estimates of sources 

of uncertainty, individually and combined. 

With this four-tiered approach, the WHO framework provides a means for systematically 

linking the characterization of uncertainty to the sophistication of the underlying risk assessment. 

Ultimately, the decision as to which tier of uncertainty characterization to include in a risk 

 

the effort to accurately characterize variability in key model inputs actually reflecting an effort to reduce 

uncertainty. 
3-9

assessment will depend both on the overall sophistication of the risk assessment and the 

availability of information for characterizing the various sources of uncertainty. 

This risk and exposure assessment for the O3 NAAQS review is relatively complex, 

possibly warranting consideration of a full probabilistic (WHO Tier 3) uncertainty analysis. For 

the exposure assessment, we include probabilistic representations of important sources of 

variability; however, due to lack of information regarding reasonable alternative parameter 

settings for model input variable distributions, we are not able to include a complete probabilistic 

analysis incorporating both variability and uncertainty. Instead, we provide sensitivity analyses 

to explore the impact of specific model assumptions, and we include a comprehensive qualitative 

discussion of uncertainty regarding the model inputs and outputs. 

While a full probabilistic uncertainty analysis is not undertaken for the epidemiologybased risk assessment due to limits in available information on distributions of model inputs, we 

provide a limited assessment using the confidence intervals associated with effects estimates 

(obtained from epidemiological studies) to incorporate statistical uncertainty associated with 

sample size considerations in the presentation of risk estimates. Technically, this type of 

probabilistic simulation represents a Tier 3 uncertainty analysis, although as noted here, it will be 

limited and only address uncertainty related to the fit of the C-R functions. Incorporation of 

additional sources of uncertainty related to key elements of C-R functions (e.g., competing lag 

structures, alternative functional forms, etc.) into a full probabilistic WHO Tier 3 analysis would 

require that probabilities be assigned to each competing specification of a given model element 

(with each probability reflecting a subjective assessment of the probability that the given 

specification is the correct description of reality). However, for most model elements there is 

insufficient information on which to base these probabilities. One approach that has been taken 

in such cases is expert elicitation; however, this approach is resource- and time-intensive, and, 

consequently, it is not feasible to use this technique in support of this O3 risk assessment. 

For most elements of the quantitative risk assessments, rather than conducting a full 

probabilistic uncertainty analysis, we include a qualitative discussion of the potential impact of 

uncertainty on risk results (WHO Tier 2). For some critical elements of the epidemiology-based 

risk assessment, e.g., the effect-estimate in the C-R function, we include sensitivity analyses to 

explore the potential impact of our assumptions. This falls under the WHO Tier 2 classification, 

although we are not able to assign probabilities to the sensitivity analyses. For these sensitivity 

analyses, we will include only those alternative specifications for input parameters or modeling 

approaches that are deemed to have scientific support in the literature (and so represent 

alternative reasonable input parameter values or modeling options). This means that the array of 

risk estimates presented in this assessment is expected to represent reasonable risk estimates that 
3-10

can be used to provide some information regarding the potential impacts of uncertainty in the 

model elements. 

3.4 CHARACTERIZATION OF AIR QUALITY 

Figure 3-1 diagrams the basic information used in developing the air quality inputs for 

the HREA. Air quality inputs to the urban area exposure and risk assessments include (1) recent 

(2006 – 2010) air quality data developed from O3 ambient monitors in each selected urban study 

area and (2) simulated air quality that reflects changes in the distribution of O3 air quality 

estimated to occur when the urban area just meets the existing or alternative O3 standards under 

consideration. In addition, O3 air quality surfaces for recent years covering the entire continental 

U.S. were generated for use in the national-scale assessment. Details of the air quality data used 

in the HREA are discussed in Chapter 4. 

Figure 3-1. Conceptual Diagram for Air Quality Characterization in the HREA. 

The urban-scale exposure and risk analyses are based on five recent years of air quality 

data, 2006-2010. We are including five years to reflect the considerable variability in 

meteorological conditions and the variation in O3 precursor emissions that have occurred in 

recent years. The analyses focus on the O3 season in each study area, which ranges from April to 

October in much of the nation but is longer in some warmer areas such as Los Angeles and 

Houston. The required O3 monitoring seasons for the urban study areas are described in more 

detail in Chapter 4. 

In developing the O3 air quality surfaces for the national-scale analysis, a combination of 

monitoring data and modeled O3 concentrations are used to provide greater coverage across the 

O3 Precursor Emissions

Ozone Air Quality Data Model-based O3 Sensitivities

O3 Metrics in Urban Case 

Study Areas: recent conditions 

and after just meeting 

existing and alternative standards

National Ambient 

O3 Spatial Fields: 

recent conditions
3-11

U.S. The procedure for fusing O3 monitor data with modeling results is described further in 

Chapter 4. 

Several O3 metrics are generated for use in the urban study area exposure and risk 

analyses. The exposure analyses use hourly O3 concentrations, while the risk analyses use 

several different averaging times. The specific metrics used in each analysis are discussed further 

in following chapters. For the exposure analysis, hourly O3 concentrations are interpolated to 

census tracts using Voronoi neighbor averaging (VNA), a distance weighted interpolation 

method (Gold, 1997; Chen et al., 2004). For the epidemiology-based risk analysis, we developed 

a composite of all monitors in the urban area for application with health effect estimates from 

epidemiology studies. We also evaluated several different definitions of the spatial boundaries of 

the urban areas that determined the monitors included in the spatial average. Some of the 

epidemiological studies specify a relatively narrow set of counties within an urban area, while 

others use a broader definition, such as all counties in a core based statistical area (CBSA) as 

defined by the Census Bureau. For those epidemiological studies that used a relatively narrow set 

of counties, most were based on counties in the center of the urban area. In most of these areas, 

the non-attaining O3 monitors are not located in the center of the urban area, but instead in the 

surrounding areas, reflecting the transport and atmospheric chemistry governing O3 formation. 

As a result, using a monitor set that exactly reflects the specific counties used in the 

epidemiology studies can exclude counties in an urban area that would realize the most risk 

reduction resulting from just meeting the O3 standard. To better represent the changes in risk that 

could be experienced in the urban areas, the core risk estimates for all endpoints will be based on 

the CBSA definition. Sensitivity analyses are included to evaluate the effect of using only the 

counties in each urban area that specifically match the county set used in the epidemiology 

studies. 

Simulation of just meeting the existing and alternative O3 standards is accomplished by 

adjusting hourly O3 concentrations measured over the O3 season using a model-based adjustment 

methodology that estimates O3 sensitivities to precursor emissions changes.6

 These sensitivities, 

which estimate the response of O3 concentrations to reductions in anthropogenic NOx and VOC 

emissions, are developed using the Higher-order Decoupled Direct Method (HDDM) capabilities 

in the Community Multi-scale Air Quality (CMAQ) model. This modeling approach incorporates 

all known emissions, including sources of natural and anthropogenic emissions in and outside of 

the U.S. By using the model-based adjustment methodology we are able to more realistically 

 

6

 In the first draft of this HREA, we used a statistical quadratic rollback approach to simulate just meeting the 

existing O3 standards. In that draft, we proposed using the model based approach that is being used in this draft, 

and received support for the model based approach from CASAC. 
3-12

simulate the temporal and spatial patterns of O3 response to precursor emissions. We chose to 

simulate just meeting the existing and alternative standards in the urban study areas by 

decreasing U.S. anthropogenic emissions of NOx exclusively, though in a few instances, 

proportional decreases in both NOx and VOC were applied. This approach was used to avoid any 

suggestion that we are approximating a specific emissions control strategy that a state or urban 

area might choose to meet a standard. More details on the HDDM-adjustment approach are 

presented in Chapter 4 of this HREA and in Simon et al. (2013).

In the previous review, background O3 (referred to in that review as policy relevant 

background, or PRB) was incorporated into the HREA by calculating risk only in excess of PRB. 

CASAC members recommended that EPA move away from using PRB in calculating risks 

(Henderson, 2007). In addition, comments received from CASAC, based on their review of the 

Risk and Exposure Assessments (Frey and Samet, 2012a; Frey, 2014), agreed with the 

development of risk estimates with reference to zero O3 concentration. Based on these 

recommendations and comments, the HREA includes risks associated with O3 from all sources 

after we have simulated just meeting the existing standard and estimates of total risk remaining 

after meeting alternative levels of the standards. EPA believes that presenting total risk is most 

relevant given that individuals and populations are exposed to total O3 from all sources, and risks 

associated with O3 exposure are due to total O3 exposure and do not vary for O3 exposure 

associated with any specific source. In addition, background O3 is fully represented in estimates 

of total risk given that the measured and adjusted air quality concentrations being used in the risk 

and exposure analyses include O3 produced from precursor emissions from both anthropogenic 

and background sources. The evidence and information on background O3 that is assessed in the 

Integrated Science Assessment (ISA) is considered in the Policy Assessment (PA) in conjunction 

with the total risk estimates provided in this HREA. With regard to background O3

concentrations, the PA will consider available information on ambient O3 concentrations 

resulting from natural sources, anthropogenic sources outside the U.S., and anthropogenic 

sources outside of North America. 

 In providing a broader national characterization of O3 air quality in the U.S., this HREA 

draws upon air quality data analyzed in the O3 ISA as well as national O3 databases and 

modeling of O3 using the Community Multiscale Air Quality (CMAQ) model. This information, 

along with additional analyses, is used to develop a broad characterization of recent air quality 

across the nation. This characterization includes O3 levels in the urban study areas for the time 

periods relevant to the risk analysis and information on the spatial and temporal characterization 

of O3 across the national monitoring network. This information is then used to place the relative 

comparative attributes of the selected study areas into a broader national comparative context to 

help judge the overall representativeness of the selected study areas in characterizing O3 risk for 
3-13

the nation. In addition, to better characterize the spatial patterns of responses of the distribution 

of O3 to just meeting existing and alternative O3 standards, we also provide assessments of the 

historical patterns of responses of O3 to emissions changes over time and an assessment of 

national patterns of responses to emissions changes relative to the spatial distribution of 

populations. These analyses are presented in more detail in Chapter 8 and Chapter 8 appendices. 

3.5 CHARACTERIZATION OF URBAN-SCALE HUMAN EXPOSURE 

Figure 3-2 diagrams the basic structure of the population exposure assessment. Basic 

inputs to the exposure assessment include the following: (1) recent (2006 - 2010) measurements 

of O3 concentrations from monitors in each selected urban study area; (2) model adjusted O3

concentrations that reflect changes in the distribution of O3 air quality estimated to occur when 

an area just meets the existing or alternative O3 standards under consideration; (3) population and 

demographic information, e.g., age, gender, etc.; (4) time-location activity pattern data; and (5) 

physiological data, e.g., body mass index, ventilation rates, lifestage development, etc. Basic 

outputs include numbers and percent of people with O3 exposures exceeding health-based 

benchmark levels and time-series of O3 exposures and ventilation rates for individuals (for use in 

the lung function risk analysis). Details of the exposure modeling are discussed in Chapter 5. 

Figure 3-2. Conceptual Diagram for Population Exposure Assessment. 

O3 Air Quality for Recent Conditions, 

and After Just Meeting Existing 

and Alternative Standards

Estimation of O3

Exposure 

Concentrations

Population and 

Demographic Information

Time Activity 

Pattern Data

Physiological 

Data

Number and % of persons with 8-

hour average exposures at or 

above selected benchmark level 

per year while at moderate or 

greater exertion

Time-series of O3 exposure 

concentrations and ventilation 

rate for individuals
3-14

The scope of the exposure assessment includes 15 urban study areas.7

 These areas were 

selected to be generally representative of U.S. populations, geographic areas, climates, and 

different O3 and co-pollutant levels, and they include all of the urban study areas used in the 

epidemiology-based risk analysis (see Chapter 7). Three additional urban study areas are 

included in the exposure modeling beyond those included in the epidemiology-based risk 

analysis. These urban study areas are included to provide additional information on 

heterogeneity in exposure but could not be included in the epidemiology-based risk analysis 

because those analyses require additional information not available in the three additional urban 

study areas. In addition to providing population exposures for estimation of lung function effects, 

the exposure modeling provides a characterization of urban air pollution exposure environments 

and activities resulting in the highest exposures. 

Population exposure to ambient O3 levels is evaluated using version 4.5 of EPA’s APEX 

model. Exposures are estimated using recent ambient O3 concentrations, based on 2006-2010 air 

quality data, and for O3 concentrations resulting from simulations of just meeting the existing 8-

hr O3 standard and alternative O3 standards, based on adjusting 2006-2010 air quality data. 

Because the O3 standard is based on the 3-year average of the 4th highest daily maximum 8-hr 

average O3 concentration, we simulate just meeting the standard for two three-year periods, 

2006-2008 and 2008-2010. Eight-hour average O3 exposures of interest in this assessment are 

based on results of controlled human exposure studies indicating adverse health effects 

associated with of 60, 70 and 80 ppb (section 2.2.5). The occurrence of exposure at or above 

these health effect benchmark levels are estimated for all school-age children (ages 5 to 18), 

asthmatic school-age children, asthmatic adults (ages 19 to 95), and older adults (ages 65 to 95). 

This choice of population groups includes a strong emphasis on children, asthmatics, and people 

≥ 65 years old and reflects the finding of the last O3 NAAQS review (U.S. EPA, 2007a,b,c) and 

the ISA (U.S. EPA, 2013a, Chapter 8) that these are important at-risk groups. 

In addition to estimating the frequency of population exposures exceeding health-based 

exposure benchmarks, estimated exposures are used as an input to the portion of the health risk 

assessment that is based on E-R relationships derived from controlled human exposure studies. 

The exposure analysis also provides a characterization of people with high exposures in terms of 

exposure environments and activities. In addition, the exposure analysis offers key observations 

 

7

 These urban study areas are Atlanta, GA; Baltimore, MD; Boston, MA; Chicago, IL; Cleveland, OH; Dallas, TX; 

Denver, CO; Detroit, MI; Houston, TX; Los Angeles, CA; New York, NY; Philadelphia, PA; Sacramento, CA; St. 

Louis, MO; and Washington, D.C. We also considered included Seattle; however, the available monitoring data 

was not sufficient to accurately characterize O3 exposures in the Seattle area. 
3-15

based on the results of the APEX modeling, viewed in the context of factors such as averting 

behavior and key uncertainties and limitations of the exposure modeling. 

3.6 CHARACTERIZATION OF URBAN-SCALE HEALTH RISKS BASED ON 

CONTROLLED HUMAN EXPOSURE STUDIES 

The major components in the lung function risk assessment are shown in Figure 3-3. 

Basic inputs to the analysis include (1) individual exposure to ambient O3 derived from the 

exposure modeling described in Section 3.5., (2) data from controlled human exposure studies, 

used to construct E-R functions, (3) physiological data, including body mass index, age, etc., and (4) 

exercise levels, which determine breathing rates and affect dose. Basic outputs include the percentage 

of a selected study group, e.g., children with asthma, with predicted lung function decrements 

(measured as decrements in forced expiratory volume in one second, or FEV1), greater than or equal 

to 10, 15, and 20 percent, for recent (2006-2010) O3 levels and for O3 levels adjusted to just meeting 

existing and alternative standards. 

Figure 3-3. Conceptual Diagram of O3 Lung Function Health Risk Assessment Based on 

Controlled Human Exposure Studies. 

Prior EPA O3 risk assessments have included risk estimates for lung function decrements 

and respiratory symptoms based on analysis of individual data from controlled human exposure 

studies. The current assessment applies probabilistic E-R relationships that are based on analyses 

Exposure Estimates: 

Individual and Population

Lung Function

Exposure-Response 

Models

Data from controlled 

human exposure studies

Physiological 

parameters

Exercise levels 

and duration

% of population with ∆FEV1>10,15,20%

for recent O3 and after just meeting 

existing and alternative standards
3-16

of individual data that describe the relationship between a measure of personal exposure to O3

and the measure(s) of lung function recorded in the study. The current quantitative lung function 

risk assessment presents only a partial picture of the risks to public health associated with shortterm O3 exposures, as there are additional controlled human exposure studies that have evaluated 

cardiovascular and neurological outcomes due to O3 exposure. However, these studies do not 

provide sufficient information with which to generate E-R functions and therefore are not 

suitable for quantitative risk assessment. Furthermore, additional adverse health response 

indicators have been measured in a number of studies, such as markers of inflammation indicated 

by the presence of neutrophils in bronchoalveolar lavage fluid (e.g., Devlin et al., 1991; see U.S. 

EPA, 2013a, section 5.3.3). However, the use of generally higher exposures observed to generate 

a significant response (> 80 ppb) and the limited number of studies reporting such information 

prevent the development of an E-R function considered useful in quantitatively estimating health 

risks associated with these additional adverse health endpoints in this assessment. 

Modeling of risks of lung function decrements is also performed by APEX using a risk 

module developed using results from controlled human exposure studies. These studies involve 

volunteer subjects, most often healthy adults, who are exposed to specified levels of O3 under 

controlled conditions for specified amounts of time, all while engaged in different exercise 

regimens. The responses measured in such studies have included measures of lung function, such 

as forced expiratory volume in one second (FEV1), respiratory symptoms, airway hyperresponsiveness, and inflammation. In addition to estimating lung function decrements for healthy 

adults that were the study groups in the controlled human exposure studies, this lung function 

risk assessment estimates lung function decrements (≥ 10, ≥ 15, and ≥ 20% changes in FEV1) in 

school-age children (ages 5 to 18). The lung function estimates for children are based on 

applying data from young adult study subjects (ages 18 to 35) to school-age children. This is 

based on findings from other chamber studies and summer camp field studies documented in the 

1996 O3 Staff Paper (U.S. EPA, 1996a) and 1996 O3 Criteria Document (U.S. EPA, 1996b), that 

lung function changes in healthy children are similar to those observed in healthy young adults 

exposed to O3 under controlled chamber conditions. Further, model-estimated lung function 

decrements using the current risk model were similar to those from a controlled clinical study of 

children ages 8-11, further supporting this approach (McDonnell et al., 1985; see 6.4.2 for 

details). Risk metrics estimated for lung function risk include the number and percent of all 

school-age children and other study groups experiencing one or more occurrences of a lung 

function decrement ≥ 10, ≥ 15, and ≥ 20% in an O3 season and the total number of occurrences 

of these lung function decrements in school-age children and active school-age children. 

The risk assessment includes two different modeling approaches. The first approach 

employs a model that estimates FEV1 responses for individuals associated with short-term 
3-17

exposures to O3 (McDonnell et al., 2012). This model is based on the data from controlled 

human exposure studies included in the prior lung function risk assessment as well as additional 

data sets that considered different measurement averaging times and breathing rates of study 

subjects. These data were from 23 controlled human O3 exposure studies that included exposure 

of 742 young adult volunteers (ages 18 to 35) (see McDonnell et al., 2007, 2010, and 2012, for a 

description of these data). Outputs from this model include FEV1 decrements for each simulated 

individual for each day, which can be used to calculate the distribution of FEV1 decrements for 

the study group, and the percent of the study group having FEV1 decrements ≥ 10, ≥ 15, and ≥

20% after air quality is adjusted to just meet the existing and alternative standards. The results 

generated using this individual-based lung function risk modeling approach are the core results 

reported in this portion of the risk assessment. 

In addition, for the purpose of comparison to previous lung function decrement modeling, 

we are applying the approach used in the last review that employed a probabilistic populationlevel E-R function derived from the results of a number of controlled human exposure studies 

(U.S. EPA, 2007a). This modeling approach uses a smaller set of controlled human exposure 

studies from which the E-R functions were derived and uses the population distribution of O3

exposures (not individual exposures) to directly estimate the percent of the population with 

moderate levels of exertion with lung function decrements ≥ 10, ≥ 15, and ≥ 20%. 

Because controlled human exposure studies are conducted in laboratory settings, they are 

generally not restricted to particular conditions that might be unique to a select geographic 

location (e.g., meteorology). Thus, the health results from controlled human exposure studies can 

appropriately be applied to any study area for which there are adequate air quality data on which 

to base the modeling of personal exposures. For this assessment, we have selected 15 urban 

study areas (matching the areas used in the exposure analysis), representing a range of 

geographic areas, population demographics, and O3 climatology. These 15 areas also include the 

12 urban study areas evaluated in the risk analyses based on C-R relationships developed from 

epidemiological or field studies. 

In the controlled human exposure study based risk assessment, there are two broad 

sources of uncertainty to the risk estimates. One of the important sources of uncertainty is the 

estimation of the population distribution of individual time series of O3 exposures and ventilation 

rates; these uncertainties are addressed as part of the exposure assessment. The second broad 

source of uncertainty in the risk calculation results from uncertainties in the lung function risk 

model. Sensitivity analyses are conducted to inform a qualitative discussion of these 

uncertainties. 
3-18

3.7 CHARACTERIZATION OF URBAN-SCALE HEALTH RISK BASED ON 

EPIDEMIOLOGICAL STUDIES 

The major components of the portion of the urban-scale health risk assessment based on 

data from epidemiological studies are illustrated in Figure 3-4. Basic inputs to this analysis 

include (1) measured O3 concentrations for recent (2007 and 2009) conditions and adjusted air 

quality representing O3 concentrations after just meeting existing and alternative standards, (2) 

C-R functions derived from epidemiological studies evaluating associations between O3

concentrations and mortality and morbidity endpoints and (3) population counts and baseline 

incidence rates for mortality and morbidity endpoints. Basic outputs for each urban area include 

estimates of O3-attributable incidence and percent O3-attributable incidence for selected 

mortality and morbidity endpoints and changes and percent changes in O3-attributable incidence. 

Figure 3-4. Conceptual Diagram of Urban-Scale Health Risk Assessment Based on Results 

of Epidemiology Studies. 

Epidemiological and field studies provide estimated C-R relationships based on data 

collected in —ambient concentration settings. Ambient O3 concentrations used in these studies 

are typically spatial averages of monitor-specific measurements, using population-oriented 

monitors. Population health responses associated with ambient O3 have included population 

counts of school absences, emergency room visits, hospital admissions for respiratory and 

cardiac illness, respiratory symptoms, and premature mortality. Risk assessment based on 

epidemiological studies typically requires baseline incidence rates and population data for the 

O3 Air Quality for Recent Conditions, 

and After Just Meeting Existing 

and Alternative Standards

BenMAP estimation of O3

Attributable Incidence of Mortality

Location-specific Short-term And Morbidity 

Exposure C-R Functions

From Epidemiological Studies

Urban Area Population and 

Baseline Health Data

Urban Area Estimates of O3

attributable incidence of mortality 

and morbidity and change in O3

attributable incidence

Urban Area Estimates of % 

O3 Attributable Incidence and 

Change in % O3 attributable 

Incidence of mortality and morbidity 

National Long-term Exposure 

C-R Functions from 

Epidemiological Studies
3-19

risk assessment study areas. To minimize uncertainties introduced by extrapolation, a risk 

assessment based on epidemiological studies can be performed for the study areas in which the 

original epidemiological studies were carried out, rather than extrapolating results to study areas 

where studies for a particular health endpoint have not been conducted. 

The set of urban study areas included in this portion of the risk assessment was chosen to 

provide population coverage and to capture the observed heterogeneity in O3-related risk across 

selected urban study areas. In addition, study areas had to have at least one epidemiological 

study conducted in order for the study area to be included for a specific endpoint. This 

assessment also evaluates the mortality risk results for the selected urban study areas within a 

broader national context to better characterize the nature, magnitude, extent, variability, and 

uncertainty of the public health impacts associated with O3 exposures. This national-scale 

assessment is discussed in the next section. 

The risk assessment based on application of results of epidemiological studies is 

implemented using the environmental Benefits Mapping and Analysis Program (BenMAP, 

version 4.0 (U.S. EPA, 2013b), EPA’s GIS-based computer program for the estimation of health 

impacts associated with air pollution. BenMAP draws upon a database of population, baseline 

incidence, ambient concentration data, and effect estimates (regression coefficients) to automate 

the calculation of health impacts. We selected 2007 and 2009 as analysis years for the urbanscale risk analysis. These two years are the midpoint years in the two three-year periods 2006-

2008 and 2008-2010. Year 2007 represents a year with generally higher O3 concentrations, and 

2009 represents a year with generally lower O3 concentrations. Analyses for these two years will 

provide a reasonable representation of the effects of baseline O3 concentrations on the risk 

estimates. 

This risk assessment is focused on health effect endpoints for which the weight of the 

evidence as assessed in the O3 ISA supports the causal determination that a likely causal or 

causal relationship exists between a specific health effect category and exposure to O3. The 

analysis includes estimates of mortality risk associated with daily maximum 8-hr average or 

means of daily 8-hr average O3 concentrations in all 12 urban study areas, as well as risk of 

hospitalization for chronic obstructive pulmonary disease and pneumonia. In addition, the 

analysis includes analysis of hospitalizations for additional respiratory diseases in Los Angeles, 

New York City, and Detroit, due to limited availability of epidemiological studies including 

these endpoints across the 12 urban areas. The analysis also evaluates risks of respiratory related 

emergency department visits in Atlanta and New York City and risks of respiratory symptoms in 

Boston, again based on limited availability of epidemiological studies that included these 

particular endpoints in their analyses and that were conducted in the same urban study areas 
3-20

evaluated in this risk assessment. Table 3-1 summarizes the endpoints evaluated for each of the 

12 urban study areas. 

Table 3-1. Short-term O3 Exposure Health Endpoints Evaluated in Urban Study Areas. 

Urban Study 

Area Mortality 

COPD1 and 

Pneumonia 

Hospitalizations 

Other 

Respiratory 

Hospitalizations 

Respiratory 

Related ED1

visits 

Respiratory 

Symptoms 

Atlanta, GA X X X 

Baltimore, MD X X 

Boston, MA X X X 

Cleveland, OH X X 

Denver, CO X X 

Detroit, MI X X X 

Houston, TX X X 

Los Angeles, CA X X X 

New York, NY X X X X 

Philadelphia, PA X X 

Sacramento, CA X X 

St. Louis, MO X X 

1

 COPD - chronic obstructive pulmonary disorder; ED - hospital emergency department. The specific health 

endpoints evaluated in our assessment for particular study areas are for where appropriate response measurements 

were made in the original epidemiological studies, i.e., most studies did not evaluate the relationship between 

ambient O3 and other respiratory hospitalizations, respiratory related ED visits, and respiratory symptoms. 

This analysis will also estimate the respiratory mortality risks associated with longer-term 

exposures to O3. This is supported by the O3 ISA, which concluded that the evidence for longterm exposures to O3 as likely to be causally related to respiratory effects, including respiratory 

mortality and morbidity. There is one national study of long-term exposures and respiratory 

mortality that provides a C-R function for use in our risk assessment. Several other studies have 

examined long-term exposures and cardiopulmonary mortality, but consistent with the O3 ISA, 

we focused on respiratory mortality because of the additional supporting evidence related to 

long-term exposure and morbidity. Because the long-term exposure C-R function is based on 

comparing O3 and mortality across urban areas, the same C-R function is applied in each of the 

12 urban study areas. The available epidemiological studies evaluating long-term O3 exposures 

and morbidity endpoints do not provide information that can be used to develop suitable C-R 

functions. As a result, we are not including quantitative risk estimates for morbidity associated 

with long-term exposures. 
3-21

We have identified multiple options for specifying the C-R functions for particular health 

endpoints. This risk assessment provides an array of reasonable estimates for each endpoint 

based on the available epidemiological evidence. This array of results provides a limited degree 

of information on the variability and uncertainty in risk due to differences in study designs, 

model specification, and analysis years, amongst other differences. 

As part of the risk assessment, we address both uncertainty and variability. We provide a 

limited probabilistic characterization of uncertainty in the national-scale mortality risk estimates 

using the confidence intervals associated with effects estimates (obtained from epidemiological 

studies). However, this addresses only one source of uncertainty. For other sources of 

uncertainty, we include a number of sensitivity analyses to evaluate the impact of alternative 

approaches to simulating just meeting existing and alternative standards, alternative C-R 

functions, definitions of O3 seasons to which C-R functions are applied, and definitions of urban 

areas to which the C-R functions are applied. In addition, we evaluate the impact in a subset of 

locations of using co-pollutant C-R functions. In the case of variability, we identify key sources 

of variability associated with O3 risk (for both short-term and long-term exposure-related 

endpoints included in the risk assessment) and discuss the degree to which these sources of 

variability are reflected in the design of the risk assessment. Finally, we also include a 

comprehensive qualitative assessment of uncertainty and variability. 

We also provide a representativeness analysis (see Chapter 8) designed to support the 

interpretation of risk estimates generated for the set of urban study areas included in the risk 

assessment. The representativeness analysis focuses on comparing the urban study areas to 

national-scale distributions for key O3-risk related attributes (e.g., demographics including 

socioeconomic status, air-conditioning use, baseline incidence rates and ambient O3 levels). The 

goal of these comparisons is to assess the degree to which the urban study areas provide 

coverage for different regions of the country as well as for areas likely to experience elevated O3-

related risk due to their specific mix of O3-risk related attributes. 

3.8 NATIONAL-SCALE MORTALITY RISK ASSESSMENT 

The major components of the national-scale mortality risk assessment are shown in 

Figure 3-5. Basic inputs to this analysis are similar to those for the urban-scale epidemiologybased assessment and include (1) gridded O3 concentrations over the continental U.S. for recent 

(2007) conditions, (2) C-R functions relating long-term and short-term exposures to O3 to 

mortality, and (3) population and baseline mortality rates. Basic outputs include county and 

national estimates of incidence and percent of mortality attributable to O3. 
3-22

The national-scale mortality risk assessment serves two primary purposes. First, it serves 

as part of the representativeness analysis discussed above, providing an assessment of the degree 

to which the urban study areas included in the risk assessment provide coverage for areas of the 

country expected to experience elevated mortality rates due to O3-exposure. Second, it provides a 

broader perspective on the distribution of risks associated with recent O3 concentrations 

throughout the U.S., and provides a more complete understanding of the overall public health 

burden associated with O3.

8

 We note that a national-scale assessment such as this was completed 

for the risk assessment supporting the latest PM NAAQS review (U.S. EPA, 2010b) with the 

results of the analysis being used to support an assessment of the representativeness of the urban 

study areas assessed in the PM NAAQS risk assessment, as described here for O3. 

 

Figure 3-5. Conceptual Diagram of National O3 Mortality Risk Assessment Based on 

Results of Epidemiology Studies. 

The national-scale risk assessment focuses on mortality only, due to the availability of 

large multi-city epidemiology studies for short-term mortality and the availability of a long-term 

mortality study which provides information to develop a suitable C-R function. As noted in the 

 

8

 In the previous O3 NAAQS review, CASAC commented that “There is an underestimation of the affected 

population when one considers only twelve urban “Metropolitan Statistical Areas” (MSAs). The CASAC 

acknowledges that EPA may have intended to illustrate a range of impacts rather than be comprehensive in their 

analyses. However, it must be recognized that O3 is a regional pollutant that will affect people living outside these 

12 MSAs, as well as inside and outside other urban areas.” Inclusion of the national-scale mortality risk 

assessment partially addresses this concern by providing a broader characterization of risk for an important O3

health endpoint. 

County and national level

estimates of burden of premature 

mortality attributable to O3

BenMAP estimation of O3

Attributable Incidence of Mortality

Nationwide Set of City 

Specific Short-term Exposure 

C-R Functions from 

Epidemiological Studies

Nationwide County Specific 

Population and Baseline 

Health Data

National ambient O3

12 km2 gridded spatial field 

for recent conditions

County and national level 

estimates of % of total mortality 

attributable to O3

National Long-term Exposure

C-R Functions from 

Epidemiological Studies
3-23

discussion of the urban-scale analyses, the available epidemiological studies evaluating longterm O3 exposures and morbidity endpoints do not provide information that can be used to 

develop suitable C-R functions. In the case of short-term morbidity endpoints, the available 

epidemiological studies are generally located in only a few urban areas and, even in the case of 

the multi-city hospitalization studies, cover only a small fraction of the urban areas in the U.S. In 

addition, baseline mortality rates are available for every county in the U.S., while baseline 

hospitalization rates are available in only a small subset of counties. For these reasons, the 

national-scale risk assessment includes only mortality associated with short- and long-term O3

exposures. 

We provide a limited probabilistic characterization of uncertainty in the national-scale 

mortality risk estimates using the confidence intervals associated with effects estimates 

originally obtained from epidemiological studies. However, this addresses only one source of 

uncertainty. To address some other key potential sources of uncertainty in the national-scale 

assessment, we conduct sensitivity analyses. Risk estimates are provided for two alternative C-R 

functions for short-term exposure, reflecting two multi-city epidemiological studies. For shortterm exposure-related mortality, the assessment provides several estimates of national mortality 

risk, including a full national-scale estimate including all counties in the continental U.S., and an 

analysis restricted to the set of urban areas included in the time-series studies that provide the 

effect estimates. We have greater confidence in the analysis based on the large urban areas 

included in the epidemiological studies, but the information from the full analysis of all counties 

is useful to gain understanding of the potential magnitude of risk in less urbanized areas. In 

addition, the national-scale mortality risk assessment evaluates the sensitivity of the nationwide 

estimates to assumptions about the transferability of effect estimates from the cities included in 

the underlying epidemiological studies to other cities in the U.S. Finally, the assessment includes 

a sensitivity analysis evaluating the use of regional priors city--rather than using a national prior 

in developing the city specific Bayesian adjusted effect estimates.9

 These sensitivity analyses are 

described in detail in Chapter 8. 

The national-scale risk assessment is conducted only for recent O3 conditions. We do not 

attempt to simulate nationwide O3 concentrations that would result from just meeting the existing 

or alternative O3 standards everywhere in the U.S. Such a simulation would require detailed 

modeling of attainment strategies in all potential non-attainment areas and would need to take 

into account the interdependence of O3 concentrations across urban areas. This type of analysis is 

 

9

 In multi-city Bayesian analyses, it is necessary to specify initial values or “priors” which are then “updated” using 

information from the individual city specific estimates. These priors are generally a mean value across all of the 

cities, in this case, cities in regions or cities across the nation. 
3-24

beyond the scope of this current risk assessment. Analyses of nationwide attainment are included 

as part of the Regulatory Impact Analyses that accompany proposed and final rulemaking 

packages and will likely be included in the rulemaking portion of this review. 

3.9 PRESENTATION OF EXPOSURE AND RISK ESTIMATES TO INFORM THE 

OZONE NAAQS POLICY ASSESSMENT 

We present exposure estimates in three ways: person-occurrences, number, and percent 

of people in different study groups (e.g., asthmatic adults, all school-age children, asthmatic 

school-age children, older adults) with at least one 8-hr average exposure at or above benchmark 

levels of 60 ppb, 70 ppb, and 80 ppb. In addition, the same types of results are shown for people 

experiencing multiple 8-hr average O3 exposures at or above the benchmark levels. The results 

are presented in summary tables and graphics, while detailed tables of results are provided in an 

appendix. The focus in the presentation of results is on exposures occurring after simulating just 

meeting the existing standard and on the change in number and percent of exposures between 

meeting the existing standard and meeting alternative standards. Results are presented for the 

five modeled years, for all 15 urban study areas. 

Quantitative risk estimates from the analyses based on application of results from 

controlled human exposure studies are presented for the two different risk models. For each 

model, we provide estimates of the percent of different study groups (all school-age (5-18) 

children, asthmatic children, and adults) with lung function decrements greater than or equal to 

10, 15, and 20 percent. As with exposure, the focus in the presentation of results is on risk 

occurring after simulating just meeting the existing standards and on the change in risk occurring 

between meeting the existing standard and meeting alternative standards. 

Results from the epidemiology-based risk assessment are presented in two ways: (1) total 

(absolute) health effects incidence for recent air quality and simulations of air quality just 

meeting the existing and alternative standards under consideration and (2) risk reduction 

estimates, reflecting the change in the distribution of O3 between scenarios of just meeting the 

existing standard and just meeting alternative standards. In addition, risks are presented as the 

percent of baseline incidence, and risks per 100,000 population, to allow for comparisons 

between urban areas with very different population sizes. We include risk modeled across the 

full distribution of O3 concentrations, as well as core risk estimates for O3 concentrations down 

to 0 ppb. 

We present an array of risk estimates in order to provide additional context for 

understanding the potential impact of uncertainty on the risk estimates. For core estimates and 

sensitivity analyses, we provide the statistical confidence intervals, demonstrating the relative 
3-25

precision of estimates. The graphical presentation of sensitivity analyses focuses on the 

differences from the core estimates in terms of risk per 100,000 population. 

The results of the representativeness analysis are presented using cumulative probability 

plots (for the national-level distribution of O3 risk-related parameters) with the locations where 

the individual urban study areas fall within those distributions noted in the plots using vertical 

lines. Similar types of plots are used to present the distribution of national-scale mortality 

estimates based on the national-scale risk assessment, showing the location of the urban study 

areas within the overall national distribution. 

Chapter 9 of this risk and exposure assessment provides a synthesis of the results from 

the four assessments (urban-scale exposure, urban-scale lung function risk, urban-scale 

epidemiology-based risk, and national-scale mortality risk). Chapter 9 focuses on comparing 

patterns of results across locations, years, and alternative standards. Chapter 9 also provides 

perspective on the overall degree of confidence of the analyses and the representativeness of the 

set of results in characterizing patterns of exposure and risk and patterns of changes in exposure 

and risk from just meeting alternative standards relative to just meeting the existing standards. 

 
3-26

3.10 REFERENCES 

Chen, J., R. Zhao and Z. Li. 2004. Voronoi-based k-order neighbor relations for spatial analysis. 

ISPRS J Photogrammetry Remote Sensing. 59(1-2), 60-72. 

Devlin, R.B.; W.F McDonnell; R. Mann; S. Becker; D.E. House; D. Schreinemachers; H.S. 

Koren. 1991. Exposure of humans to ambient levels of ozone for 6.6 hours causes 

cellular and biochemical changes in the lung. American Journal of Respiratory Cell and 

Molecular Biology. 4(1):72-81. 

Frey, C. and J. Samet. 2012a. CASAC Review of the EPA’s Health Risk and Exposure Assessment 

for Ozone (First External Review Draft - Updated August 2012) and Welfare Risk and 

Exposure Assessment for Ozone (First External Review Draft - Updated August 2012). U.S. 

Environmental Protection Agency Science Advisory Board. EPA-CASAC-13-002. 

Frey, C. and J. Samet. 2012b. CASAC Review of the EPA’s Policy Assessment for the Review 

of the Ozone National Ambient Air Quality Standards (First External Review Draft – 

August 2012). U.S. Environmental Protection Agency Science Advisory Board. EPACASAC-13-003. 

Frey, C. 2014. CASAC Review of the EPA’s Health Risk and Exposure Assessment for Ozone 

(Second External Review Draft – February, 2014). U.S. Environmental Protection Agency 

Science Advisory Board. EPA-CASAC-14-005. 

Gold, C. 1997. Voronoi methods in GIS. In: Algorithmic Foundation of Geographic Information 

Systems (va Kereveld M.; J. Nievergelt; T. Roos; P. Widmayer, eds.). Lecture Notes in 

Computer Science, Vol 1340. Berlin: Springer-Verlag, pp 21-35. 

Henderson, R. 2007. Clean Air Scientific Advisory Committee’s (CASAC) Review of the 

Agency’s Final O3 Staff Paper. EPA-CASAC-07-002. March 26, 2007. 

Langstaff, J.E. 2007. OAQPS Staff Memorandum to Ozone NAAQS Review Docket (EPA HQOAR-2005-0172). Subject: Analysis of Uncertainty in Ozone Population Exposure 

Modeling. [January 31, 2007]. 

<http://www.epa.gov/ttn/naaqs/standards/ozone/data/2007-

01_o3_exposure_uncertainty.pdf >. 

McDonnell, W.F.; R.S. Chapman; M.W. Leigh; G.L. Strope; and A.M. Collier. 1985. 

Respiratory responses of vigorously exercising children to 0.12 ppm ozone exposure. 

American Review of Respiratory Disease. 132:875-879. 

McDonnell, W.F.; P.W. Stewart and M.V. Smith. 2007. The temporal dynamics of ozone–

induced FEV1 changes in humans: an exposure-response model. Inhalation Toxicology. 

19:483–494. 

McDonnell W.F.; P.W. Stewart and M.V. Smith. 2010. Prediction of O3 -induced lung function 

responses in humans. Inhalation Toxicology, 22(2):160-8. 

McDonnell, W.F.; P.W. Stewart; M.V. Smith; C.S. Kim and E.S. Schelegle. 2012. Prediction of 

lung function response for populations exposed to a wide range of ozone conditions. 

Inhalation Toxicology. 24: 619-633. 

Samet, J. 2009. Consultation on EPA’s Draft Integrated Review Plan for the National Ambient 

Air Quality Standards for Particulate Matter. (EPA document number EPA-CASAC-10-

004. December 3). 
3-27

Samet, J. 2011. Consultation on EPA’s O3 National Ambient Air Quality Standards: Scope and 

Methods Plan for Health Risk and Exposure Assessment (April 2011) and Ozone 

National Ambient Air Quality Standards: Scope and Methods Plan for Welfare Risk and 

Exposure Assessment (April 2011). EPA-CASAC-11-008. June 21. 

Simon H.; K.R. Baker; F. Akhtar; S.L. Napelenok; N. Possiel; B. Wells and B. Timin. 2013. A 

direct sensitivity approach to predict hourly ozone resulting from compliance with the 

national ambient air quality standard. Environmental Science and Technology. 

47(5):2304-13. 

U.S. EPA. 1996a. Review of National Ambient Air Quality Standards for Ozone: Assessment of 

Scientific and Technical Information - OAQPS Staff Paper. (EPA document number 

EPA/452/R-96-007). Research Triangle Park, NC: Office of Air Quality Planning and 

Standards. Available from: NTIS, Springfield, VA; PB96–203435. < 

http://www.epa.gov/ttn/naaqs/standards/ozone /s_O3_pr.html>. 

U.S. EPA. 1996b. Air Quality Criteria for Ozone and Related Photochemical Oxidants. (EPA 

document number EPA/600/P-93/004aF-cF). Research Triangle Park, NC: Office of 

Research and Development, National Center for Environmental Assessment. 

<http://cfpub.epa.gov/ ncea/cfm/recordisplay.cfm?deid=2831>. 

 U.S. EPA. 2007a. Ozone Population Exposure Analysis for Selected Urban Areas. Research 

Triangle Park, NC: Office of Air Quality Planning and Standards. (EPA document 

number EPA-452/R-07-010). 

<http://www.epa.gov/ttn/naaqs/standards/ozone/data/2007_07_o3_exposure_tsd.pdf>. 

U.S. EPA. 2007b. Ozone Health Risk Assessment for Selected Urban Areas. Research Triangle 

Park, NC: Office of Air Quality Planning and Standards. (EPA document number EPA 

452/R-07-009). 

<http://www.epa.gov/ttn/naaqs/standards/ozone/data/ozone_ra_final_tsd_7-2007.pdf>. 

U.S. EPA. 2007c. Review of the National Ambient Air Quality Standards for Ozone: Policy 

Assessment of Scientific and Technical Information. OAQPS Staff Paper. Research 

Triangle Park, NC: Office of Air Quality Planning and Standards. (EPA report 

numberEPA-452/R-07-007. 

<http://www.epa.gov/ttn/naaqs/standards/ozone/data/2007_07_ozone_staff_paper.pdf>. 

U.S. EPA. 2008. Risk and Exposure Assessment to Support the Review of the NO2 Primary 

National Ambient Air Quality Standard. (EPA document number EPA-452/R-08-008a). 

<http://www.epa.gov/ttn/naaqs/standards/nox/data/20081121_NO2_REA_final.pdf>. 

U.S. EPA. 2009a. Integrated Review Plan for the Ozone National Ambient Air Quality Standards 

Review: External Review Draft. Research Triangle Park, NC: Environmental Media 

Assessment Group, National Center for Environmental Assessment and Health and 

Environmental Impacts Division, Office of Air Quality Planning and Standards. (EPA 

document number EPA 452/D-09-001). 

U.S. EPA. 2009b. Risk and Exposure Assessment to Support the Review of the SO2 Primary 

National Ambient Air Quality Standard. EPA Office of Air Quality Planning and 

Standards. (EPA document number EPA-452/R-09-007). 

<http://www.epa.gov/ttn/naaqs/standards/so2/data/200908SO2REAFinalReport.pdf.> 

U.S. EPA. 2010a. Quantitative Risk and Exposure Assessment for Carbon Monoxide – Amended. 

EPA Office of Air Quality Planning and Standards. (EPA document number EPA-452/R-
3-28

10-009, July). <http://www.epa.gov/ttn/naaqs/standards/co/data/CO-REA-AmendedJuly2010.pdf>. 

U.S. EPA. 2010b. Quantitative Health Risk Assessment for Particulate Matter. Research 

Triangle Park, NC: Office of Air Quality Planning and Standards. (EPA document 

number EPA-452/R-10-005). 

<http://www.epa.gov/ttn/naaqs/standards/pm/data/PM_RA_FINAL_June_2010.pdf>. 

U.S. EPA. 2011a. Integrated Review Plan for the O3 National Ambient Air Quality Standards. 

Research Triangle Park, NC: National Center for Environmental Assessment, Office of 

Research and Development and Office of Air Quality Planning and Standards, Office of 

Air and Radiation. (EPA document number EPA 452/R-11-006). 

<http://www.epa.gov/ttn/naaqs/standards/ozone/data/2011_04_OzoneIRP.pdf>. 

U.S. EPA. 2011b. Ozone National Ambient Air Quality Standards: Scope and Methods Plan for 

Health Risk and Exposure Assessment. Research Triangle Park, NC: Office of Air 

Quality Planning and Standards. (EPA document number EPA-452/P-11-001). < 

http://www.epa.gov/ttn/naaqs/standards/ozone/data/2011_04_HealthREA.pdf>. 

U.S. EPA. 2011c. Ozone National Ambient Air Quality Standards: Scope and Methods Plan for 

Welfare Risk and Exposure Assessment. Research Triangle Park, NC: Office of Air 

Quality Planning and Standards. (EPA document number EPA-452/P-11-002). 

U.S. EPA. 2013a. Integrated Science Assessment of Ozone and Related Photochemical Oxidants 

(Final Report). Research Triangle Park, NC: EPA Office of Research and Development. 

(EPA document number EPA/600/R-10/076F). 

U.S. EPA. 2013b. Environmental Benefits Mapping Analysis Program (BenMAP v4.0). Posted 

January, 2013. < http://www.epa.gov/air/benmap/download.html />. 

Wegman, L. 2012. Updates to information presented in the Scope and Methods Plans for the O3

NAAQS Health and Welfare Risk and Exposure Assessments. Memorandum from Lydia 

Wegman, Division Director, Health and Environmental Impacts Division, Office of Air 

Quality Planning and Standards, Office of Air and Radiation, US EPA to Holly 

Stallworth, Designated Federal Officer, Clean Air Scientific Advisory Committee, US 

EPA Science Advisory Board Staff Office. May 2, 2012. 

WHO. 2008. World Health Organization Harmonization Project Document No. 6. Part 1: 

Guidance Document on Characterizing and Communicating Uncertainty in Exposure 

Assessment. <http://www.who.int/ipcs/methods/harmonization/areas/exposure/en/.>. 
4-1 

4 AIR QUALITY CHARACTERIZATION 

4.1 INTRODUCTION 

Air quality information is used in Chapter 5 through Chapter 8 to assess risk and 

exposure resulting from recent O3 concentrations, as well as to estimate the relative change in 

risk and exposure that could result from just meeting the existing O3 standard of 75 ppb and the 

potential alternative standard levels of 70 ppb, 65 ppb, and 60 ppb.1 The same air quality data are 

used to examine fifteen2 urban study areas in the population exposure analyses discussed in 

Chapter 5 and the lung function risk assessment based on application of results from clinical 

studies discussed in Chapter 6: Atlanta, GA; Baltimore, MD; Boston, MA; Chicago, IL; 

Cleveland, OH; Dallas, TX; Denver, CO; Detroit, MI; Houston, TX; Los Angeles, CA; New 

York, NY; Philadelphia, PA; Sacramento, CA; St. Louis, MO; and Washington, DC. The 

epidemiology-based risk assessment discussed in Chapter 7 examines twelve3 of the fifteen 

urban study areas evaluated in the population exposure analyses. Finally, Chapter 8 includes an 

assessment of the national-scale O3 mortality risk burden associated with recent O3

concentrations, and characterizes the representativeness of the 15 urban study areas compared to 

the rest of the U.S. This chapter describes the air quality information developed for these 

analyses, providing an overview of monitoring data and air quality (section 4.2) and an overview 

of air quality inputs to the risk and exposure assessments (section 4.3). 

4.2 OVERVIEW OF OZONE MONITORING AND AIR QUALITY DATA 

To determine whether or not the NAAQS have been met at an ambient O3 monitoring 

site, a statistic commonly referred to as a “design value” must be calculated based on three 

consecutive years of data collected from that site. The form of the existing O3 NAAQS design 

value statistic is the 3-year average of the annual 4th highest daily maximum 8-hour (8-hr) O3

concentration in parts per billion (ppb), with decimal digits truncated. The existing primary and 

secondary O3 NAAQS are met at an ambient monitoring site when the design value is less than 

or equal to 75 ppb.4

 In counties or other geographic areas with multiple monitors, the area-wide 

 

1

 For a subset of urban areas and analyses, the HREA evaluates a standard level of 55 ppb, consistent with 

recommendations from CASAC to also give consideration to evaluating a level somewhat below 60 ppb. 2

 In the first draft REA, we proposed to include 16 urban areas in the second draft REA. However, further analysis 

of the air quality information available for Seattle, WA has prompted us to not include that city. This decision and 

supporting analysis are discussed in more detail in Appendix 4E. 3

 These study areas are Atlanta, GA; Baltimore, MD; Boston, MA; Cleveland, OH; Denver, CO; Detroit, MI; 

Houston, TX; Los Angeles, CA; New York, NY; Philadelphia, PA; Sacramento, CA; and St. Louis, MO. 4 For more details on the data handling procedures used to calculate design values for the existing O3 NAAQS, see 

40 CFR Part 50, Appendix P. 
4-2 

design value is defined as the design value at the highest individual monitoring site, and the area 

is said to have met the NAAQS if all monitors in the area are meeting the NAAQS. 

Air quality monitoring data from 1,468 U.S. ambient O3 monitoring sites were retrieved 

by EPA staff for use in the risk and exposure assessments. The initial dataset consisted of hourly 

O3 concentrations in ppb collected between 1/1/2006 and 12/31/2010 from these monitors. Data 

for nearly 1,400 of these monitors were extracted from EPA’s Air Quality System (AQS) 

database5, while the remaining data came from EPA’s Clean Air Status and Trends Network 

CASTNET) database which consists of primarily rural monitoring sites. 

These data were split into two design value periods, 2006-2008 and 2008-2010, and all 

subsequent analyses based on these data were conducted independently for these two periods. 

Observations flagged in AQS as having been affected by exceptional events were included the 

initial dataset, but were not used in design value calculations in accordance with EPA’s 

exceptional events policy. Missing data intervals of 1 or 2 hours in the initial dataset were filled 

in using linear interpolation. These short gaps often occur at regular intervals in the ambient data 

due to an EPA requirement for monitoring agencies to perform routine quality control checks on 

their O3 monitors. Quality control checks are typically performed between midnight and 6:00 

AM when O3 concentrations are low. Missing data intervals of 3 hours or more were not 

replaced. Interpolated data values were not used in design value calculations. 

Figure 4-1 and Figure 4-2 show the design values for the existing O3 NAAQS for all 

regulatory monitoring sites in the U.S. for the 2006-2008 and 2008-2010 periods, respectively. In 

general, O3 design values were lower in 2008-2010 than in 2006-2008, especially in the Eastern 

U.S. There were 518 O3 monitors in the U.S. with design values above the existing standard in 

2006-2008, compared to only 179 in 2008-2010. 

 

5 EPA’s Air Quality System (AQS) database is a national repository for many types of air quality and related 

monitoring data. AQS contains monitoring data for the six criteria pollutants dating back to the 1970’s, as well as 

more recent additions such as PM2.5 speciation, air toxics, and meteorology data. At present, AQS receives 

hourly O3 monitoring data collected from nearly 1,400 monitors operated by over 100 state, local, and tribal air 

quality monitoring agencies. 
4-3 

Figure 4-1. Map of Monitored 8-hr O3 Design Values for the 2006-2008 Period. 

Figure 4-2. Map of Monitored 8-hr O3 Design Values for the 2008-2010 Period. 
4-4 

4.3 OVERVIEW OF URBAN-SCALE AIR QUALITY INPUTS TO RISK AND 

EXPOSURE ASSESSMENTS 

The air quality information input into the urban-scale risk and exposure assessments 

includes both recent air quality data from the years 2006-2010, as well as air quality data 

adjusted to reflect just meeting the existing and potential alternative standard levels. In this 

section, we summarize these air quality inputs and discuss the methodology used to adjust air 

quality to meet the existing and potential alterative standards. Figure 4-3 presents a flowchart of 

air quality data processing steps for the urban-scale analyses. The rest of section 4.3.1 will 

provide more details on each step depicted in the flow diagram. Additional information is 

provided in Appendices 4A, 4B and 4D. 

Figure 4-3. Flowchart of Air Quality Data Processing for Different Parts of the Urbanscale Risk and Exposure Assessments. 
4-5 

4.3.1 Urban Study Areas 

4.3.1.1 Exposure modeling and controlled human exposure study-based risk 

assessment 

The 15 urban study areas in the exposure modeling and lung function risk assessments 

covered a large spatial extent, with boundaries generally similar to those covered by the 

respective Combined Statistical Areas (CSA) defined by the U.S. Census Bureau. Table 4-1 

gives some basic information about the 15 urban study areas in the exposure assessment, 

including the number of ambient monitoring sites, the required O3 monitoring season, and the 

2006-2008 and 2008-2010 design values for each study area. All 15 of the urban study areas had 

8-hr O3 design values above the existing standard in 2006-2008, while 13 urban areas had 8-hr 

O3 design values above the existing standard in 2008-2010. Chicago (74 ppb) and Detroit (75 

ppb) had design values meeting the existing standard during the 2008-2010 period. The design 

values in the 15 urban areas decreased by an average of 6 ppb between 2006-2008 and 2008-

2010, ranging from no change in Sacramento to a decrease of 15 ppb in Atlanta. 

Table 4-1. Monitor and Area Information for the 15 Urban Study Areas in the Exposure 

Modeling and Clinical Study Based Risk Assessment. 

Study Area 

# of 

Counties 

# of O3

Monitors 

Population 

(2010) 

Required O3

Monitoring Season 

2006-2008 

DV (ppb) 

2008-2010 

DV (ppb)

Atlanta 33 13 5,618,431 March - October 95 80 

Baltimore 7 7 2,710,489 April - October 91 89 

Boston 10 14 5,723,468 April - September 83 77 

Chicago 16 26 9,686,021 April - October 78 74 

Cleveland 8 13 2,881,937 April - October 82 77 

Dallas 11 20 6,366,542 January - December 89 86 

Denver 13 26 3,390,504 March - September 86 77 

Detroit 9 12 5,218,852 April - September 81 75 

Houston 10 22 5,946,800 January - December 91 85 

Los Angeles 5 54 17,877,006 January - December 119 112 

New York 27 31 21,056,173 April - October 90 84 

Philadelphia 15 19 7,070,622 April - October 92 83 

Sacramento 7 26 2,755,972 January - December 102 102 

St. Louis 17 17 2,837,592 April - October 85 77 

Washington DC 26 22 5,838,518 April - October 87 81 

Because O3 design values are based on the annual 4th highest daily maximum 8-hr 

average O3 concentrations from 3-consecutive years, it is useful to look at inter-annual 

variability. In general, the annual 4th highest 8-hr O3 concentrations decreased in 11 of the 15 

urban areas from 2006 to 2010, while remaining relatively constant in the other 4 areas (Figure 

4-4). The average decrease in the annual 4th highest daily maximum concentration from 2006 to 

2010 was 8 ppb. However, there was significant year-to-year variability, and some areas showed 

increases in some years relative to 2006, even though the 2010 values were generally lower. 
4-6 

Figure 4-4. Trends in Annual 4th Highest Daily Maximum 8-hr Average O3 Concentrations 

in ppb for the 15 Urban Study Areas for 2006-2010. Urban areas are grouped into 3 

regions: Eastern (top), Central (middle), and Western (bottom). 
4-7 

4.3.1.2 Epidemiological-based risk assessment 

Table 4-2 gives some basic information on the 12 urban study areas in the epidemiologybased risk assessment for each set of area boundaries. The spatial extent of each urban study area 

was based on the respective Core Based Statistical Area (CBSA)6

. The CBSAs were generally 

smaller than the study areas used in the exposure modeling and clinical study based risk 

assessments, except for Baltimore and Houston, where the two study areas were identical. The 

rationales for the definitions of the spatial areas used in each type of analysis are provided in the 

corresponding chapters. The final two columns in Table 4-2 show the annual 4th highest daily 

maximum 8-hr O3 concentration in ppb for the monitors within each urban study area in 2007 

and 2009. 

It should be noted that the CBSA boundaries used for the urban study areas in this 

assessment are different than those used in the 1st draft of the HREA, where the study areas were 

derived from the Zanobetti and Schwartz (2008) study. The change to the CBSA boundaries was 

intended to capture a larger portion of the urban area populations by including some surrounding 

suburban counties, rather than focusing strictly on the urban population centers. Two sensitivity 

analyses were conducted to determine the effect of changing the spatial extent of the urban study 

areas on the epidemiology-based risk estimates. These sensitivity analyses are presented in 

Chapter 7, and a summary of the two alternative sets of boundaries for the 12 urban study areas 

are provided in Appendix 4A. 

Since O3 is not directly emitted but is formed through photochemical reactions, precursor 

emissions may continue to react and form O3 downwind of emissions sources, thus the highest 

O3 concentrations are often found downwind of the highest concentrations of precursor 

emissions near the urban population center. There were some instances where the highest 

monitor occurred outside of the CBSA, but within the exposure area, which was designed to 

always include the monitor associated with the area-wide design value. For example, in Los 

Angeles, the CBSA includes Los Angeles and Orange counties, but the highest O3 concentrations 

are typically measured further downwind in Riverside and San Bernardino counties. Thus, the 

values reported in Table 4-2 may not match the values shown in Figure 4-4. 

 

 

6

 Core Based Statistical Areas (CBSAs) are used by the Office of Management and Budget (OMB) to group U.S. 

counties into urbanized areas. These groupings are updated by OMB every 5 years. The CBSAs used in the 

epidemiology based risk assessment are based on the OMB delineations from 2008. For more information see: 

http://www.whitehouse.gov/sites/default/files/omb/assets/bulletins/b10-02.pdf
4-8 

Table 4-2. Monitor and Area Information for the 12 Urban Study Areas in the 

Epidemiology Based Risk Assessment. 

Study Area 

# of 

Counties 

# of O3

Monitors 

Population 

(2010) 

2007 4th high 

(ppb) 

2009 4th high 

(ppb)

Atlanta 28 13 5,268,860 102 77 

Baltimore 7 7 2,710,489 92 83 

Boston 7 11 4,552,402 89 75 

Cleveland 5 10 2,077,240 83 72 

Denver 10 16 2,543,482 97 79 

Detroit 6 8 4,296,250 93 73 

Houston 10 22 5,946,800 90 91 

Los Angeles 2 21 12,828,837 105 108 

New York 23 22 18,897,109 94 81 

Philadelphia 11 15 5,965,343 102 74 

Sacramento 4 17 2,149,127 93 96 

St. Louis 16 17 2,812,896 94 74 

4.3.2 Recent Air Quality 

The sections below summarize the recent air quality data input into the epidemiological 

study-based risk assessment, and the exposure and controlled human exposure study-based risk 

assessment. Additional details on these inputs are provided in Appendix 4A. 

4.3.2.1 Exposure modeling and controlled human exposure study based risk 

assessment 

As discussed in more detail in Chapter 5, the HREA uses the Air Pollutants Exposure 

(APEX) model (U.S. EPA, 2012a, b) to simulate exposure and to estimate lung function 

decrements based on application of results of controlled human exposure studies to populations 

in the 15 urban study areas. The APEX model uses spatial fields of hourly O3 concentrations at 

each census tract within an urban area to simulate exposure. We use Voronoi Neighbor 

Averaging (VNA) (Gold, 1997; Chen et al, 2004) to estimate hourly O3 concentrations at each 

census tract in all 15 urban study areas, for recent measured air quality, air quality meeting the 

existing standard of 75 ppb, and air quality meeting potential alternative standards.7

 The VNA 

fields were estimated using ambient hourly O3 concentrations from monitors in each urban area, 

as well as monitors within a 50 km buffer region around the boundaries of each area. Additional 

details on the procedure used to generate the VNA fields, and a technical justification for the 

change from nearest neighbor fields to VNA fields are included in Appendix 4A. 

 

7

 In the first draft REA, these hourly spatial fields were generated for four urban areas using the concentrations from 

the nearest neighboring O3 monitor. 
4-9 

Figure 4-5 shows county-level maps of the 15 urban study areas. Counties colored pink 

indicate the study area boundaries used in the Zanobetti & Schwartz (2008) and/or Smith et al. 

(2009b) studies,8 where applicable. Counties colored gray indicate additional counties within the 

CBSA boundaries, and counties colored peach indicate any additional counties included in the 

exposure and lung function risk assessments. The X’s indicate locations of the O3 monitors used 

in the risk and exposure assessments, including those within the 50 km buffer region used to 

create the VNA fields. 

4.3.2.2 Epidemiology-based risk assessment 

We input O3 air quality concentration data for the epidemiology-based risk analyses into 

the environmental Benefits Mapping and Analysis Program (BenMAP) (U.S. EPA, 2013) for 

assessment. We used BenMAP to analyze four different daily O3 metrics in 12 of the 15 urban 

study areas, which were the basis for concentration-response relationships derived in various 

epidemiology studies: 

(1) Daily maximum 1-hr concentration 

(2) Daily maximum 8-hr concentration 

(3) Daytime 8-hr average concentration (10:00AM to 6:00PM) 

(4) Daily 24-hr average concentration 

The air quality monitoring data used in BenMAP were daily time-series of “composite 

monitor” values for each of the 12 urban areas for years 2007 and 2009, which were chosen to 

represent years with high and low O3 concentrations, respectively. The composite monitor values 

were calculated by first averaging the hourly O3 concentrations for all monitors within the areaof-interest (resulting in a single hourly time-series for each urban area), then calculating the four 

daily metrics listed above. More details on the composite monitor value calculations and a 

presentation of the resulting concentrations can be found in Appendices 4A and 4D, respectively. 

 

8

 The Zanobetti and Schwartz (2008) and Smith et al (2009) study area boundaries were identical for 6 of the 12 

urban study areas, and had at least one county in common for all 12 urban study areas. The ‘Epidemiology Study 

Area’ labels in Figure 4-5 refer to counties included in either of these two studies. 
4-10 

Figure 4-5a. Maps of the 5 Eastern U.S. Urban Study Areas Including O3 Monitor 

Locations. 
4-11 

Figure 4-5b. Maps of the 5 Central U.S. Urban Study Areas Including O3 Monitor 

Locations. 
4-12 

Figure 4-5c. Maps of the 5 Western U.S. Urban Study Areas Including O3 Monitor 

Locations. 
4-13 

4.3.3 Air Quality Adjustments for Just Meeting Existing and Potential Alternative Ozone 

Standards 

The focus of the risk and exposure assessments is the evaluation of risks and exposures 

after just meeting existing and alternative standards, and the change in risk between just meeting 

existing standards and just meeting alternative standards. These evaluations require estimation of 

the change in hourly O3 concentrations that may occur in each urban area when “just meeting” 

the existing and potential alternative O3 standards. 

The first draft HREA and the previous O3 NAAQS review used the “quadratic rollback” 

method to adjust ambient O3 concentrations to simulate just meeting existing and alternative 

standards (U.S. EPA, 2007; Wells et al., 2012). Although the quadratic rollback method 

replicates historical patterns of air quality changes better than some alternative methods (e.g. 

simply shaving peak concentrations off at the NAAQS level and the proportional rollback 

technique), its implementation relies on a statistical relationship instead of on a mechanistic 

characterization of physical and chemical processes in the atmosphere. Because of its construct 

as a statistical fit to measured O3 values, the quadratic rollback technique cannot capture spatial 

and temporal heterogeneity in O3 response and also cannot account for nonlinear atmospheric 

chemistry that causes increases in O3 during some hours and in some locations as a result of 

emissions reductions under some circumstances. 

Photochemical grid models are better able to simulate these phenomena and therefore the 

first draft HREA proposed to replace quadratic rollback with a model-based O3 adjustment 

methodology and presented a test case for Atlanta and Detroit using modeling for July/August 

2005 (Simon et al., 2012). The section below summarizes the methodology applied in this 

assessment to adjust air quality to just meet existing and alternative standards. This new 

methodology applies Higher-Order Decoupled Direct Method (HDDM) capabilities in the 

Community Multi-scale Air Quality (CMAQ) model to simulate the response of O3

concentrations to reductions in US anthropogenic NOx and VOC emissions. The model 

incorporates anthropogenic U.S., Canadian, Mexican and other international emissions, as well 

as emissions from non-anthropogenic sources. Since sources of background O3 are incorporated 

explicitly in the modeling, specifying U.S. background concentrations is unnecessary. 

Application of this approach also addresses the recommendation by the National Research 

Council of the National Academies (NRC, 2008) to explore how emissions reductions might 

affect temporal and spatial variations in O3 concentrations, and to include information on how 

NOx versus VOC control strategies might affect risk and exposure. 
4-14 

4.3.3.1 Methods 

The EPA has developed an HDDM-adjustment methodology to estimate hourly O3

concentrations that could occur at each monitor location if urban study areas were to meet the 

existing and various alternative levels of the O3 standard. An early version of this methodology 

was proposed in the first draft HREA (Simon et al., 2012) and published in a peer-reviewed 

journal (Simon et al., 2013). The methodology and its application to hourly O3 concentrations in 

the urban study areas is summarized below and described in more detail in Appendix 4D. 

The HDDM-adjustment methodology uses the CMAQ photochemical model to determine 

monitoring site-specific response of hourly O3 concentrations to reductions in US anthropogenic 

NOx and VOC emissions. The CMAQ model simulation was run for 8-months (January, AprilOctober) in 2007 and used a 12km grid resolution covering the continental United States. The 

modeled responses are then applied to ambient data to create a 5-year time-series of hourly O3

concentrations at each monitor location which is consistent with meeting various potential levels 

of the O3 NAAQS for the two three-year averaging periods 2006-2008 and 2008-2010. The steps 

are outlined in Figure 4-6 and summarized below: 

 Step 1: Run CMAQ simulation with HDDM to determine hourly O3 sensitivities to NOx

emissions and VOC emissions for the grid cells containing monitoring sites in an urban 

area. 

• Inputs: Model-ready emissions and meteorology data 

• Outputs: Ozone concentrations and sensitivities at locations of monitoring sites 

for each hour in January and April-October, 2007

 Step 2: For each monitoring site, season, and hour of the day use linear regression to 

relate first order sensitivities of NOx and VOC (SNOx and SVOC) to modeled O3 and second 

order sensitivities to NOx and VOC (S2

NOx and S2VOC) to the first order sensitivities. The 

relationships derived here are strictly empirical and the applicability of these modelderived relationships to ambient data relies on the assumption that the real-world 

relationship is captured by the model. 

• Inputs: Step 1 outputs 

• Outputs: Functions to calculate typical sensitivities based on monitor location, 

O3 concentration, season, and hour of the day

 Step 3: For each measured hourly O3 value between 2006 and 2010, calculate the first 

and second order sensitivities based on monitoring site-, season-, and hour-specific 

functions derived in Step 2. 

• Inputs: Step 2 outputs and hourly ambient data for 2006-2010. 

• Outputs: Hourly O3 observations paired with modeled sensitivities for all hours 

in 2006-2010 at all monitor locations
4-15 

 Step 4: Adjust measured hourly O3 concentrations for incrementally increasing levels of 

emissions reductions using assigned sensitivities and then recalculate design values until 

an emissions reduction level is reached at which all monitors in an urban area are below 

the existing and potential alternative levels of the standard. 

• Inputs: Step 3 outputs 

• Outputs: Adjusted hourly O3 values for 2006-2010 at monitor locations to show 

compliance with the existing and potential alternative standard levels based on the 

three year average of the 4th highest daily maximum 8-hr averageO3 value. For 

each standard, two sets of data are created: 2006-2008 and 2008-2010. Because 

the emissions reductions used to attain standards in the two time periods might be 

different, adjusted 2008 O3 values are different for the two sets of data.

 Step 5: Process hourly monitor data to create composite monitor time-series for 

epidemiology risk assessment and to create hourly VNA spatial surfaces for exposure and 

lung function risk assessment as shown in Figure 4-3.

 

Natural

Canada and 

Mexico U.S.

Anthropogenic

O3 and O3 Precursor Emissions

Recent Monitored O3

(2006-2010)

Step 1a:

CMAQ 

HDDM Modeling

(Jan, Apr-Oct 2007)

Meteorology

Initial and Boundary conditions

Other Model Inputs

Select Emissions 

Reductions to 

which Sensitivities 

Will Be Applied

Step 1b:

Extract Output

Step 2:

Create Regressions

Step 3:

Use Regressions and 

Observed Ozone to 

Predict Sensitivities

Step 4:

Adjust Hourly Ozone 

to Meet Alternate

Standards

Adjusted Hourly Ozone

Values for 2006-2010 at 

Each Monitor Location to

Show Attainment with

Alternate Standards 

Unique Linear 

Relationships Between 

Sensitivities and Hourly 

Ozone at Each Monitor

Location for Each 

Season and 

Hour-of-the-Day 

Hourly Ozone 

Observations Paired with

Sensitivities for 2006-2010

At All Monitor Locations 

Ozone Concentrations 

& Sensitivities at 

Locations of 

Monitoring Sites for

Each Modeled Hour 

(Jan, Apr-Oct 2007)

Gridded hourly O3 

Concentrations and 

Sensitivities

 

Figure 4-6. Flowchart of HDDM Adjustment Methodology to Inform Risk and Exposure 

Assessments. 
4-16 

The CMAQ HDDM modeling described above is used to approximate O3 response to 

emission changes and is most accurate for emissions changes smaller than 50%. To 

accommodate increasing uncertainty at larger emission adjustments, the HDDM modeling was 

performed at three distinct emissions levels (base conditions, 50% cut in NOx and/or VOC 

emissions, and 90% cut in NOx and/or VOC emissions) to allow for a better characterization of 

O3 response over the entire range of emissions levels. A detailed description of the methodology 

and evaluation for this 3-step HDDM adjustment procedure is provided in Appendix 4D. 

We chose to adjust air quality for just meeting the existing and alternative standards by 

decreasing U.S. anthropogenic emissions of NOx and/or VOC throughout the U.S. For the 

purpose of this analysis we used the Community Multiscale Air Quality (CMAQ) model version 

4.7.1 equipped with HDDM to simulate 8 months in 2007 (January and April-October). This 

time period was chosen to cover the full O3 season and also includes at least one month from 

each season of the year. A full description of the model inputs, model set-up, and operational 

model evaluation against ambient data is available in Appendix 4B. Sensitivities derived from 

the 2007 model simulation were applied to the two 3-year periods of ambient data (2006-2008 

and 2008-2010) described in section 4.3.1.1. 

By applying across-the-board decreases in anthropogenic emissions throughout the U.S., 

we were able to estimate how O3 would respond to changes in ambient NOx and/or VOC 

concentrations without simulating a specific control strategy. The model was set up to track 

response in hourly O3 concentrations to these across-the-board changes in US anthropogenic 

NOx and VOC emissions. It should be noted that although nationwide emission decreases were 

imposed, different levels of emission decreases were used for different urban study areas. In 

choosing to apply across the board reductions throughout the modeling domain, we recognize 

that not all emissions across the domain contribute equally to nonattainment in each urban area. 

However, by decreasing emissions across the domain, we allow for the possibility of 

contribution from both regional and local emissions sources to nonattainment and to the overall 

distribution of O3 concentrations in urban areas. 

The purpose of these reduction scenarios is not to evaluate the feasibility of a particular 

emission control or to account for reductions associated with other rulemakings but rather to 

develop internally consistent estimates of spatial and temporal variability in O3 associated with 

specified alternative levels of possible standards. The modeling included sources which 

contribute to background O3 such as biogenic emissions, wildfire emissions, and transport of O3

and its precursors from international source regions. In addition, the HDDM tool was set-up to 

specifically calculate the changes in O3 that would occur from changes in US anthropogenic 

emissions alone, yet to account for the effects of background sources on this response. 

Consequently, it is not necessary to set a “floor” background O3 concentration as was done for 
4-17 

quadratic rollback because background sources are explicitly accounted for in the model 

estimates of O3 response to US anthropogenic emissions. 

As described in more detail in Appendix 4D, the HDDM adjustment methodology 

estimates hourly O3 concentrations that would be associated with attaining a targeted level of the 

standard either though reductions in US anthropogenic NOx emissions alone or through 

reductions of both US anthropogenic NOx and VOC emissions in equal percentages. We 

explored the use of scenarios that reduced VOC alone, but found that O3 response due to 

reductions in anthropogenic VOC reductions alone could not adjust the air quality to just meet a 

60 ppb standard in any of the 15 urban study areas evaluated. Because the combined NOx/VOC 

cuts are constrained to equal percentage cuts of both precursors, this is not an optimized 

NOx/VOC control scenario but rather a sensitivity analysis to characterize the range of results 

that could be obtained with alternate assumptions. In most of the urban areas, although the 

NOx/VOC scenario affected O3 response on some days, it did not affect O3 response at the 

highest design value (or controlling) monitor in such a way to reduce the total required emissions 

cuts. However, for the Chicago and Denver study areas, the NOx/VOC scenarios allowed for 

lower percentage emissions cuts (applied to both NOx and VOC) to reach targeted standard 

levels than the NOx only scenario. Table 4-3 shows the percent emissions reductions applied in 

both the NOx-only and the NOx/VOC scenarios for each urban study area. Because of this, the 

core analyses presented in the remainder of this chapter and in Chapters 5, 6, and 7 were based 

on the NOx only assumption for all study areas except for Chicago and Denver which used the 

NOx/VOC equal percentage reduction assumption. Sensitivity analyses were performed to 

compare the NOx only and the NOx/VOC cases in 9 study areas: Denver, Detroit, Houston, Los 

Angeles, New York, Philadelphia, and Sacramento. The effects of these sensitivity analyses on 

air quality and on the epidemiology-based risk assessment are discussed in more detail in 

Appendix 4D and Chapter 7, respectively. 

 
4-18 

Table 4-3. NOx-only and NOx/VOC Emission Reductions Applied to 15 Urban Study 

Areas. Numbers in blue bold text represent the base scenario while numbers in plain font 

represent the scenario used in the sensitivity analyses for each urban study area. 

Study Area Years 

NOx only NOx/VOC 

75 70 65 60 75 70 65 60 

Atlanta 

2006-2008 50% 58% 64% 71% N/A N/A N/A N/A 

2008-2010 23% 43% 54% 62% N/A N/A N/A N/A 

Baltimore 

2006-2008 46% 54% 61% 69% N/A N/A N/A N/A 

2008-2010 44% 52% 60% 67% N/A N/A N/A N/A 

Boston 

2006-2008 40% 49% 61% 70% N/A N/A N/A N/A 

2008-2010 13% 40% 53% 65% N/A N/A N/A N/A 

Chicago 

2006-2008 41% 54% 65% 75% 19% 52% 66% 80% 

2008-2010 N/A 42% 56% 67% N/A 27% 55% 70% 

Cleveland 

2006-2008 48% 61% 73% 88% N/A N/A N/A N/A 

2008-2010 50% 64% 77% 88% N/A N/A N/A N/A 

Dallas 

2006-2008 50% 57% 65% 72% 51% 60% 69% 77% 

2008-2010 50% 58% 64% 71% 50% 59% 68% 76% 

Denver 

2006-2008 54% 67% 76% 89% 51% 65% 78% 87% 

2008-2010 24% 53% 70% 89% 15% 46% 64% 87% 

Detroit 

2006-2008 59% 69% 76% 84% 60% 73% 85% 90% 

2008-2010 N/A 54% 66% 78% N/A 53% 69% 85% 

Houston 

2006-2008 62% 68% 74% 82% 65% 73% 81% 87% 

2008-2010 42% 53% 63% 75% 40% 52% 65% 85% 

Los Angeles 

(95% LB) 

2006-2008 87% 89% 91% 93% 95% 96% 98% 99% 

2008-2010 87% 89% 91% 93% 93% 95% 97% 98% 

New York 

(95% LB) 

2006-2008 64% 74% 92% N/A 60% 71% 89% N/A 

2008-2010 52% 67% 89% N/A 41% 55% 86% N/A 

Philadelphia 

2006-2008 54% 61% 68% 74% 57% 65% 71% 79% 

2008-2010 42% 52% 61% 68% 37% 52% 62% 72% 

Sacramento 

2006-2008 63% 70% 76% 84% 65% 73% 80% 88% 

2008-2010 64% 71% 77% 84% 65% 74% 81% 88% 

St. Louis 

2006-2008 45% 56% 66% 75% N/A N/A N/A N/A 

2008-2010 10% 34% 50% 63% N/A N/A N/A N/A 

Washington 

D.C. 

2006-2008 53% 60% 67% 74% N/A N/A N/A N/A 

2008-2010 31% 50% 60% 71% N/A N/A N/A N/A 

 
4-19 

For New York and Los Angeles it should also be noted that a somewhat different 

approach was used for the HDDM-adjustment application. The HDDM adjustment methodology 

produces estimates of hourly O3 concentrations with standard error bounds for every potential 

emission reduction scenario. Uncertainties in the application of the methodology to very large 

emissions adjustments along with the highly nonlinear response of O3 to NOx reductions at a 

limited number of sites and hours resulted in the inability of this methodology to estimate O3

distributions in these two study areas that could just meet lower alternative standard levels (65 

ppb for New York, 60 ppb for Los Angeles). This does not indicate that these two areas would 

not be able to meet these lower standard levels in reality, but simply reveals the limitations of 

this adjustment methodology. More specifically, at a few highly urbanized monitors during some 

seasons, the O3 increases during highly titrated rush-hour and nighttime hours appear to be 

overestimated, leading to predictions that, when NOx was reduced, O3 would peak during rushhour periods on the very highest O3 days. Even at these monitors, the majority of days in the O3

season did not have this issue. To address the atypical behavior on the very highest O3 days in 

the adjustment scenarios in New York and Los Angeles, we took the 95th percentile confidence 

interval for each hourly O3 prediction and used the lower bound value to determine the NOx

reductions required to meet the existing and potential alternative standards and to calculate the 

hourly O3 that would occur under that reduced emission scenario. During most hours and at most 

monitors, the 95th percentile range was small so the use of the lower-bound of the 95th percentile 

range made little difference in predicted O3 concentrations. However, using the lower bound of 

the 95th percent confidence interval allowed us to dampen the effect of over-predicted O3

increases during rush-hour times. Since the O3 concentrations for each standard level were 

created using consistent methodology, these O3 datasets can be used to compare between 

standards in these study areas. More details are provided in Appendix 4D. Estimates of risk for 

these two study areas for these alternative standards will be significantly more uncertain, 

reflecting the use of the lower bound O3 predictions. 

4.3.3.2 Resulting air quality 

The HDDM adjustment technique tended to have several effects on the distribution of air 

quality values. First, adjusted hourly O3 concentrations at night and during the morning rushhour tended to be higher than the recent observed concentrations (additional details are provided 

in Appendix 4D). The CMAQ model predicts that, in general, these times have NOx titration 

conditions meaning that a reduction in NOx causes an increase in O3 concentrations. The NOx

titration effect was most pronounced in urban core areas which have higher volume of mobile 

source NOx emissions from vehicles than do the surrounding areas. Response of daytime 

concentrations was more varied. In general, O3 tended to increase on low days and decrease on 
4-20 

high days. However, specific monitors that were either always heavily VOC limited or always 

heavily NOx limited showed consistent increases and decreases respectively regardless of 

whether O3 concentrations were high or low on a particular day. It should be noted that locations 

which were heavily VOC limited tended to have much lower observed O3 concentrations than 

downwind areas. The tendency of the model to predict O3 increases on lower concentration days 

and decreases on higher concentration days also leads to more compressed O3 distributions in the 

HDDM adjustment cases. The variability in predicted daily O3 concentrations decreased when 

meeting lower standard levels. The following paragraphs summarize a comparison of O3

distributions from application of the quadratic rollback and HDDM adjustment approach for a 

case where the existing standard is estimated to be met, characterize the distribution of 

composite monitor O3 values at different standard levels, and provide a discussion of the spatial 

distribution of O3 changes in several study areas. More details and figures for other study areas 

are provided in Appendix 4D.

Figure 4-7 and Figure 4-8 show a comparison of April-October composite monitor O3

distributions for recent conditions (2006-2008) and for meeting the existing standard using the 

quadratic rollback technique versus the HDDM adjustment methodology. The composite monitor 

values in these plots are based on the monitors included in the composite monitor from the 

Zanobetti and Schwartz (2008) study which was used in the 1st draft HREA and do not include 

all monitors in the CBSA as used in the main Chapter 7 analysis. In general, the O3 distribution 

in the HDDM adjustment case is shifted upward compared to the quadratic rollback case. The 

upward shift is more pronounced in the lower parts of the O3 distribution. In all study areas 

displayed in Figure 4-7, the 25th percentile, median, and mean of the daily maximum 8-hr 

average O3 concentrations are higher in the HDDM adjustment case than the quadratic rollback. 

In some study areas (Sacramento and St. Louis) the 75th percentile values appear approximately 

equivalent in the two cases while in other study areas the 75th percentile values are slightly 

higher in the HDDM adjustment case. In Houston, the very highest portion of the O3 distribution 

is lower in the HDDM adjustment case than in the quadratic rollback case but in many study 

areas the upper parts of the distributions for these two cases are roughly equivalent. Similar 

results are seen in the 2008-2010 time period; however there are more cases during this time 

period where HDDM adjustment and quadratic rollback have similar values in the upper half of 

the O3 distribution. A comparison of Figure 4-7 and Figure 4-8 shows that there is some 

seasonality to this effect. The two techniques appear to give very similar daily maximum 8-hr 

averageO3 composite monitor distributions during the summer months (June-August) and most 

of the situations with higher O3 levels with the HDDM adjustment come from cooler, lower O3

time periods (April, May, September, and October). Although here we discuss composite 

monitor distributions based on April-October, the risk analyses in Chapter 7 are based on the 
4-21 

required O3 monitoring season, which is longer than April – October for some study areas. We 

expect that the O3 increases shown for spring and fall months here are also representative of the 

type of response in other “cool season” months. The exceptions to this occur in Denver, Houston, 

New York and Los Angeles which have higher composite monitor O3 values from the HDDM 

adjustment compared to quadratic rollback even in the summer time period. 

Figure 4-9 and Figure 4-10 show “box-and-whisker” plots of the April-October 

composite monitor daily maximum 8-hr average O3 concentration distributions for the 12 urban 

study areas evaluated in the epidemiology-based risk assessment; for recent air quality, and air 

quality adjusted to meet the existing and potential alternative standards. Figure 4-9 shows values 

from 2007, while Figure 4-10 shows values from 2009. Note that since these boxplots represent 

composite monitor values (i.e. an average of values from multiple individual monitors) the 

maximum composite monitor concentration may still be well below the design value which is 

measured from a single monitor in some areas. Appendix 4D contains additional plots comparing 

the changes in the distribution of composite monitor values in each urban area due to the air 

quality adjustments across varying spatial extents, season lengths, and years. In general, the 

range of the composite monitor distributions decreased (i.e. the minimum value increased, while 

the maximum value decreased) in all 12 urban study areas as the air quality data were adjusted to 

meet lower standard levels. However, the changes within the inter-quartile range of these 

distributions (represented by the “boxes”) varied in response to the model-based air quality 

adjustments across the 12 urban areas. Three different types of responses are highlighted in the 

boxplots for Atlanta, New York, and Houston. 

The Atlanta boxplots provide an example of an urban area in which all but the lowest 

composite monitor values decreased as the air quality data was adjusted to simulate compliance 

with progressively lower levels of the standard. The upper tail of the distribution (represented by 

the top whisker in each boxplot) decreased more quickly than the remainder of the distribution, 

resulting in less total variability in the composite monitor values with each progressively lower 

standard level. This type of response was also seen Sacramento and St. Louis, and to a lesser 

extent in Baltimore, Denver, and Philadelphia. 

In New York, the boxplots showed an initial increase in the 25th percentile and median 

composite monitor values when the observed O3 concentrations were adjusted to meet the 

existing standard. However, the median composite monitor value decreased relative to the 

existing standard as O3 concentrations were adjusted to meet the 70 ppb standard, and both the 

median and 25th percentile values decreased when air quality were further adjusted to meet the 

65 ppb standard. When the air quality were adjusted to meet 65 ppb, the median and mean 

composite monitor values were lower than under observed conditions. This type of response was 

also observed in Cleveland, Detroit, and Los Angeles. 
4-22 

Figure 4-7. Distributions of Composite Monitor Daily Maximum 8-hr Average O3

Concentrations from Ambient Measurements (black), Quadratic Rollback (blue), and the 

HDDM Adjustment Methodology (red) for Meeting the Existing Standard. Values are 

based on the Zanobetti & Schwartz study areas for April-October of 2006-2008. Boxes 

represent the median and quartiles, X’s represent mean values, whiskers extend up to 1.5x 

the inter-quartile range from the boxes, and circles represent outliers. 
4-23 

Figure 4-8. Distributions of Composite Monitor Daily Maximum 8-hr Average O3

Concentrations from Ambient Measurements (black), Quadratic Rollback (blue), and the 

HDDM Adjustment Methodology (red) for Meeting the Existing Standard. Values are 

based on the Zanobetti & Schwartz study areas for June-August of 2006-2008. Boxes 

represent the median and quartiles, X’s represent mean values, whiskers extend up to 1.5x 

the inter-quartile range from the boxes, and circles represent outliers. 
4-24 

Figure 4-9. Distributions of Composite Monitor Daily Maximum 8-hr Average Values for 

the 12 Urban Study Areas in the Epidemiology-based Risk Assessment. Plots depict values 

based on ambient measurements (base), and values obtained with the HDDM adjustment 

methodology when just meeting the 75, 70, 65 and 60 ppb standards. Values shown are 

based on CBSAs for April-October of 2007. Note that the HDDM adjustment technique 

was not able to adjust air quality to just meet a 60 ppb standard in New York, so no 

boxplot is shown for that case. Boxes represent the median and quartiles, X’s represent 

mean values, whiskers extend up to 1.5x the inter-quartile range from the boxes, and 

circles represent outliers. 
4-25 

Figure 4-10. Distributions of Composite Monitor Daily Maximum 8-hr Average Values for 

the 12 Urban Study Areas in the Epidemiology-based Risk Assessment. Plots depict values 

based on ambient measurements (base), and values obtained with the HDDM adjustment 

methodology when just meeting the 75, 70, 65 and 60 ppb standards. Values shown are 

based on CBSAs for April-October of 2009. Note that Detroit air quality was meeting 75 

ppb in 2008-2010, and the HDDM adjustment technique was not able to adjust air quality 

to just meet a 60 ppb standard in New York, so no boxplots are shown for those cases. 

Boxes represent the median and quartiles, X’s represent mean values, whiskers extend up 

to 1.5x the inter-quartile range from the boxes, and circles represent outliers. 
4-26 

In Houston, the median composite monitor value also increased between observed air 

quality and air quality adjusted to meet the existing standards. However, the pattern in Houston 

differed from New York and other study areas as air quality was further adjusted to reflect 

meeting the potential alternative standards. The median value remained relatively constant 

relative to the existing standard, while the 25th percentile values continued to increase. Thus, in 

Houston, the air quality adjustments always resulted in a median composite monitor value higher 

than what was seen in the observed data. The composite monitor distributions in Boston also 

exhibited this type of behavior. 

The exposure modeling and the clinical-based risk assessments used spatially varying 

surfaces of hourly O3 concentrations estimated at the centroid of each census tract within the 15 

urban study areas. The maps in Figures 4-11, 4-12, and 4-13 depict the spatial distributions of the 

2006-2008 average 4th highest (top) and May – September mean (bottom) daily maximum 8-hr 

average (MDA8) O3 concentrations for 3 of the 15 urban study areas; for observed air quality 

(left), air quality adjusted to meet the existing standard (center), and air quality adjusted to meet 

the 65 ppb alternative standard (right). Appendix 4A contains additional maps of the observed 4th

highest MDA8 and May – September mean MDA8 concentrations in all 15 urban study areas for 

2006-2008 and 2008-2010. Appendix 4D contains maps and related figures showing the changes 

in air quality that resulted from the HDDM adjustments for just meeting the existing standard, 

and just meeting the potential alternative standard of 65 ppb. 

These maps portray the general pattern seen in all 15 urban study areas for the 4th highest 

concentrations, which decreased when observed air quality were adjusted to meet the existing 

standard, and continued to decrease as the air quality were further adjusted to meet the various 

alternative standards. The May-September average values also generally decreased in suburban 

and rural areas surrounding the urban population center in all 15 areas. However, three different 

types of general behavior which were seen in the seasonal average values near the urban 

population centers, exemplified in Figures 4-11 (Atlanta), 4-12 (New York), and 4-13 (Houston). 

In Atlanta, the observed May - September average were nearly constant across the entire 

study area. The observed values decreased nearly uniformly across the entire study area when 

observed air quality was adjusted to meet the existing standard, and continued to do so when air 

quality was further adjusted to meet the alternative standard of 65 ppb. The magnitudes of these 

decreases were slightly larger in suburban and rural areas than near the urban population center. 

This type of behavior was also seen in Sacramento and Washington, D.C. 

In New York, the observed May – September average values were lower near the urban 

population center than in the surrounding suburban areas. When the observed air quality was 

adjusted to meet the existing standard, the seasonal average values increased near the urban 

population center and decreased in the suburban areas, so that the spatial pattern was reversed. 
4-27 

When air quality was further adjusted to meet the 65 ppb alternative standard, large area-wide 

decreases in the seasonal average values were seen relative to the existing standard. While New 

York represents one of the most extreme examples, similar behavior was observed in 7 other 

urban areas: Baltimore, Cleveland, Dallas, Detroit, Los Angeles, Philadelphia, and St. Louis. 

The distribution of O3 concentrations in Houston started out in a similar fashion as New 

York. The observed May – September average concentrations were lower near the urban 

population center than in the surrounding areas, and a similar pattern of increasing and 

decreasing seasonal average values occurred when observed air quality was adjusted to meet the 

existing standard. However, unlike New York, the seasonal average values near the Houston city 

center remained nearly constant relative to the existing standard when air quality were further 

adjusted to meet the 65 ppb standard. Boston, Chicago, and Denver exhibited this same type of 

behavior. 

4th Highest MDA8 ‐ Base

May ‐ Sep mean MDA8 ‐ Base

4th Highest MDA8 ‐ 75 ppb

May ‐ Sep mean MDA8 ‐ 75 ppb

4th Highest MDA8 ‐ 65 ppb

May ‐ Sep mean MDA8 ‐ 65 ppb

Atlanta, 2006 ‐ 2008

Figure 4-11. Maps Showing the 4th highest (top) and May-September Average (bottom) 

Daily Maximum 8-hr Average O3 Concentrations in Atlanta based on 2006-2008 Ambient 

Measurements (left), HDDM Adjustment to Meet the Existing Standard (center), and 

HDDM Adjustment to Meet AN Alternative Standard of 65 ppb (right). Squares represent 

measured values at monitor locations; circles represent VNA estimates at census tract 

centroids. 
4-28 

4th Highest MDA8 ‐ Base

May ‐ Sep mean MDA8 ‐ Base

4th Highest MDA8 ‐ 75 ppb

May ‐ Sep mean MDA8 ‐ 75 ppb

4th Highest MDA8 ‐ 65 ppb

May ‐ Sep mean MDA8 ‐ 65 ppb

New York, 2006 ‐ 2008

Figure 4-12. Maps Showing the 4th highest (top) and May-September Average (bottom) 

Daily Maximum 8-hr Average O3 Concentrations in New York based on 2006-2008 

Ambient Measurements (left), HDDM Adjustment to Meet the Existing Standard (center), 

and HDDM Adjustment to Meet the Alternative Standard of 65 ppb (right). Squares 

represent measured values at monitor locations; circles represent VNA estimates at census 

tract centroids. 
4-29 

4th Highest MDA8 ‐ Base

May ‐ Sep mean MDA8 ‐ Base

4th Highest MDA8 ‐ 75 ppb

May ‐ Sep mean MDA8 ‐ 75 ppb

4th Highest MDA8 ‐ 65 ppb

May ‐ Sep mean MDA8 ‐ 65 ppb

Houston, 2006 ‐ 2008

Figure 4-13. Maps of 4th Highest (top) and May-September Average (bottom) Daily 

Maximum 8-hr Average O3 Concentrations in Houston for 2006-2008 Ambient 

Measurements (left), HDDM Adjustment to Meet the Existing Standard (center), and 

HDDM Adjustment to Meet the Alternative Standard of 65 ppb (right). Squares represent 

measured values at monitor locations; circles represent VNA estimates at census tract 

centroids. 

Figures displaying the air quality results from the NOx-only compared to the NOx/VOC 

adjustment scenarios are provided in Appendix 4D. Comparison of the composite monitor and 

spatial plot maps leads to several general conclusions for this sensitivity analysis. First, the 

NOx/VOC reduction scenarios tended to mitigate increases that occurred in the NOx-only 

scenario at the lower end of the O3 concentration distribution. Second the effect on the NOx/VOC 

scenario versus the NOx-only scenario was less dramatic for mid-range O3 concentrations and 

varied from study area to study area. The NOx/VOC scenarios lead to lower mid-range O3

concentrations than the NOx-only scenarios except in the case of New York. Third, the high end 

O3 concentrations at various standard levels were similar in the NOx-only and the NOx/VOC 

scenarios. Finally, the VOC reductions tended to have more impact in urban core areas and 
4-30 

relatively little impact in outlying areas. The effects of these air quality sensitivity analyses on 

risk are evaluated and discussed in chapter 7. 

4.4 OVERVIEW OF NATIONAL-SCALE AIR QUALITY INPUTS 

The national-scale analysis, presented in Chapter 8, is focused only on evaluating the 

total national burden of mortality risk associated with recent O3 conditions. As such it uses a 

different approach to characterize air quality conditions throughout the U.S. The national-scale 

analysis employs a data fusion approach that takes advantage of the accuracy of monitor 

observations and the comprehensive spatial information of the CMAQ modeling system to create 

national-scale “fused” spatial surfaces of seasonal average O3 concentrations. Measured O3

concentrations from 2006-2008 were fused with modeled concentrations from a 2007 CMAQ 

model simulation, run for a 12 km domain covering the contiguous U.S. The spatial surfaces are 

created using EPA’s Downscaler software (Berrocal et al., 2012). More details on the ambient 

measurements, the 2007 CMAQ model simulation, and the Downscaler fusion technique can be 

found in Appendix 4C.9

Three national “fused” spatial surfaces were created for: 

(1) the May-September mean of the daily maximum 8-hr average O3 concentrations 

(consistent with the metric used by Smith et al. 2009); 

(2) the June-August mean of the daily 10am-6pm average O3 concentrations (consistent 

with the metric used by Zanobetti and Schwartz 2008); and 

(3) the April-September mean of the daily maximum 1-hour O3 concentrations 

(consistent with the metric used by Jerrett et al 2009). 

Figure 4-14 to Figure 4-16 show the geographic distributions of these spatial surfaces. 

The spatial distributions of these three surfaces are very similar, with the highest levels occurring 

in Southern California for all three surfaces. 

 

9

 In the first draft of the REA, the spatial surfaces were created using the enhanced Voronoi Neighbor Averaging 

(eVNA) technique (Timin et al, 2010), using the EPA’s Model Attainment Test Software (MATS; Abt Associates, 

2010b). The technical justification for changing from eVNA to Downscaler can be found in Appendix 4C. 
4-31 

Figure 4-14. May-September Mean of the Daily Maximum 8-hr Average O3

Concentrations in ppb, based on a Downscaler Fusion of 2006-2008 Average Monitored 

Values with a 12km 2007 CMAQ Model Simulation. 
4-32 

Figure 4-15. June-August Average 8-hr Daily 10am-6pm Mean O3 Concentrations in ppb, 

based on a Downscaler Fusion of 2006-2008 Average Monitored Values with a 12km 2007 

CMAQ Model Simulation. 
4-33 

Figure 4-16. April-September Mean of the Daily Maximum 1-hr O3 Concentrations in ppb, 

based on a Downscaler Fusion of 2006-2008 Average Monitored Values with a 12km 2007 

CMAQ Model Simulation. 

Figure 4-17 shows the frequency and cumulative distributions of these three seasonal 

average O3 surfaces based on all grid cells in the 12 km CMAQ modeling domain. The 

minimum, median, mean, 95th percentile, and maximum values for all three surfaces are shown 

in Table 4-4, and correlation coefficients between the three metrics are given in Table 4-5. 

The May-September mean of the daily maximum 8-hr average O3 concentrations were 

most frequently in the 30-60 ppb range, while the June-August average daily 10am–6pm mean 

concentrations were more evenly distributed across a range of 20-60 ppb. The April-September 

mean of the daily maximum 1-hr O3 concentrations were about 5 ppb higher on average than the 

May-September mean daily maximum 8-hr average concentrations, and about 8 ppb higher on 

average than the June-August average daily 10am-6pm mean concentrations. The correlation 

coefficients between these three metrics were all very high (R > 0.97). 
4-34 

Figure 4-17. Frequency and Cumulative Distributions of the Three Fused Seasonal 

Average O3 Surfaces Based on all CMAQ 12 km Grid Cells. 
4-35 

Table 4-4. Summary Statistics based on the Three Fused Seasonal Average O3 Surfaces 

Based on all CMAQ 12 km Grid Cells. 

Statistic 

May-September mean 

of the daily maximum 

8-hr average 

concentration (ppb) 

June-August mean of the 

daily 10am–6pm average 

concentration (ppb) 

April-September mean 

of the daily maximum 1-

hr concentration (ppb) 

Minimum 21.8 14.9 26.2 

Median 43.6 41.7 48.8 

Mean 43.2 40.9 48.2 

95th Percentile 54.3 54.8 59.0 

Maximum 76.1 80.1 84.2 

Table 4-5. Correlation Coefficients between the Three Fused Seasonal Average O3

Surfaces Based on all CMAQ 12 km Grid Cells. 

Seasonal metrics compared Correlation coefficient 

May-September mean of the daily maximum 8-hr average 

vs. June-August mean of the daily 10am-6pm average 0.974 

May-September mean of the daily maximum 8-hr average 

vs. April-September mean of the daily maximum 1-hr 0.995 

June-August mean of the daily 10am-6pm average vs. 

April-September mean of the daily maximum 1-hr 0.972 

These seasonal average metrics are not equivalent to the form of the existing standard, 

which is based on the 4th highest value rather than on the seasonal mean. Thus, the values shown 

in the three fused surfaces should not be directly compared to the existing standard. Figure 4-18 

shows comparisons between these three metrics and the 2006-2008 O3 design values based on 

CMAQ 12 km grid cells containing O3 monitors, and Table 4-6 presents correlation coefficients 

and summary statistics based on the ratios between the design values and these three metrics. 

The design values were, on average, approximately 50% higher than the seasonal average values, 

with substantial spatial heterogeneity, and some variation across the seasonal average metrics. 

The April-September mean of the daily maximum 1-hr O3 concentration was the most strongly 

correlated with the design values (R = 0.75), followed by the May-September mean of the daily 

maximum 8-hr average (R = 0.71), and then the June-August mean of the daily 10am-6pm 

average O3 concentration (R = 0.69). 
4-36 

Figure 4-18. 2006-2008 O3 Design Values Versus 2006-2008 Fused Seasonal Average O3

Levels for the CMAQ 12km Grid Cells Containing O3 Monitors. 
4-37 

Table 4-6. Correlation Coefficients and Ratios of the 2006-2008 O3 Design Values to the 

2006-2008 Fused Seasonal Average O3 Levels for the CMAQ 12km Grid Cells Containing 

O3 Monitors. 

Statistic 

May-September mean of 

the daily maximum 8-hr 

average 

June-August mean of 

the daily 10am-6pm 

average 

April-September mean 

of the daily maximum 1-

hr 

Correlation 0.71 0.69 0.75 

Ratios 

Minimum 1.1 1.1 1.0 

2.5th Percentile 1.3 1.3 1.2 

Median 1.5 1.5 1.4 

Mean 1.6 1.6 1.4 

97.5 Percentile 2.0 2.2 1.6 

Maximum 2.4 3.0 1.9 

4.5 UNCERTAINITIES IN MODELING OF RESPONSES TO EMISSION 

REDUCTIONS TO JUST MEET EXISTING AND POTENTIAL ALTERNATIVE 

STANDARDS 

We recognize that there are sources of uncertainty in air quality measurements and the air 

quality estimates for each air quality scenario. These sources of uncertainty are described below 

and in Table 4-7 which discusses qualitatively the magnitude of uncertainty and potential for 

directional bias. 

There is inherent uncertainty in all deterministic air quality models, such as CMAQ, the 

photochemical grid model which was used to develop the model-based O3 adjustment 

methodology. Evaluations of air quality models against observed pollutant concentrations build 

confidence that the model performs with reasonable accuracy despite both structural and 

parametric uncertainties. A comprehensive model performance evaluation provided in Appendix 

4B shows generally acceptable model performance which is equivalent to or better than typical 

state-of-the science regional modeling simulations as summarized in Simon et al. (2012). The 

use of the Higher Order Decoupled Direct Method (HDDM) within CMAQ to estimate O3

response to emissions perturbations adds uncertainty to that inherent in the model itself. HDDM 

allows for the approximation of O3 concentrations under alternate emission scenarios without rerunning the model simulation with different inputs. This approximation becomes less accurate 

for larger emissions perturbations. To accommodate increasing uncertainty at larger emissions 

perturbations, the HDDM modeling was performed at three distinct emissions levels to allow for 

a better characterization of O3 response over the entire range of emissions levels. The accuracy 

of the HDDM estimates can be quantified at distinct emissions levels by re-running the model 

with modified emissions inputs and comparing the results. This method was applied to quantify 
4-38 

the accuracy of 3-step HDDM O3 estimates for 50% and 90% NOx cut conditions for each urban 

study areas (as shown in Appendix 4D). At 50% NOx cut conditions, HDDM using information 

from these multiple simulations predicted hourly O3 concentrations with a mean bias and a mean 

error less than +/- 1 ppb in all urban study areas compared to brute force model simulations. At 

90% NOx cut conditions, HDDM using information from these multiple simulations predicted 

hourly O3 concentrations with a mean bias less than +/- 3ppb and a mean error less than +/- 4 

ppb in all urban study areas. These small bias and error estimates show that uncertainty due to 

the HDDM approximation method is small up to 90% emissions cuts. 

In order to apply modeled O3 response to ambient measurements, regressions were 

developed which relate O3 response to emissions perturbations with ambient O3 concentrations 

for every season, hour-of-the-day, and monitor location. These regressions are purely empirical 

so applying O3 responses to ambient data based on this modeled relationship adds uncertainty. 

Preliminary work showed that the relationships developed with these regressions were generally 

statistically significant for most season, hour-of-the-day, and monitor location combinations for 

2005 modeling in Detroit and Charlotte (Simon et al., 2012). Statistical significance was not 

evaluated for each regression in this analysis since there were over 460,000 regressions created 

(322 monitors × 5 sensitivity coefficients × 3 emissions levels × 4 seasons × 24 hours = 463,680 

regressions). Statistical inference can quantify the goodness of fit for the modeled relationships. 

The regression model provided both a central tendency and a standard error value representing 

the uncertainty in the central tendency at any at any given O3 concentration. Appendix 4D 

provides equations used to calculate the standard error values and propagate them through the 

calculations of hourly and daily maximum 8-hr average O3 values for each adjustment scenario. 

Since emissions reductions increased for lower standard levels the standard errors were larger for 

adjustments to lower standards. Mean (95th percentile) standard errors for the 75 ppb adjustment 

case ranged from 0.13 (0.26) to 1.18 (2.87) ppb for hourly O3 concentrations in the 15 urban 

study areas. Mean (95th percentile) standard errors for the 65 ppb adjustment case ranged from 

0.54 (1.07) to 1.39 (2.98) ppb for hourly O3 concentrations. The largest standard errors occurred 

in Los Angeles and New York due to the large emissions reductions applied in these cases. 

Figures 4-19 and 4-20 show the range of standard errors in daily maximum 8-hr average O3

values for each of the 15 urban study areas based on the uncertainty predicting the central 

tendency from the regressions. These boxplots show that standard error from this source is 

generally small (less than 1 ppb) in all urban study areas. There are infrequent occurances of 

larger standard errors shown by the X’s denoting maximum standard error on any day in Figure 

4-19. The maximum standard error on any day is still in the range of 1-3 ppb in most urban study 

ares but is higher in Denver, New York and Los Angeles for the 60 ppb scenarios. Maps of mean 

standard error at each monitor location are provided in Appendix 4D. 
4-39 

The base analysis in all urban study areas except New York and Los Angeles used the 

central tendency which will inherently dampen some of the variability in O3 response. This may 

lead to an underestimation of the variability of O3 concentration decreases and increases 

associated with emission reductions but is not expected to lead to a bias in estimated benefits. 

However, given the small standard error values even in the urban study areas with the greatest 

uncertainty (i.e. less than 1.5 ppb mean standard error), this source of uncertainty is not expected 

to substantially impact exposure and risk results. 

Figure 4-19. Propagated Standard Error in Daily Maximum 8-hr Average O3

Concentrations Due to Uncertainty in Linear Regression Central Tendency for Each 

Urban Study Area. Boxes show the interquartile range while whiskers extent to 1.5x the 

interquartile range, X’s show mina and max values. 
4-40 

Figure 4-20. Propagated Standard Error in Daily Maximum 8-hr Average O3

Concentrations Due to Uncertainty in Linear Regression Central Tendency for Each 

Urban Study Area. Boxes show the interquartile range while whiskers extent to 1.5x the 

interquartile range. Note that this is the same as Figure 4-19 above except with Y-axis 

adjusted. 

Relationships between O3 response and hourly O3 concentration are empirical and were 

developed based on 8 months of modeling: January and April-October 2007. These relationships 

were applied to ambient data from 2006-2010. This relies on the assumption that relationships 

between O3 response and O3 concentration, hour of day, location, and season in the real world 

are well replicated in the model. Since it is not possible to directly measure O3 response in the 

real-world we rely on the fact that the statistical fit was generally good for the modeled 

relationships and the model performed reasonably well at predicting hourly and daily maximum 

8-hr average O3 concentrations in 2007. In addition to the general uncertainties introduced by 

applying empirical modeled relationships to ambient O3 data, uncertainty is also introduced 

because these relationships are applied outside of the modeled time period. Some locations 

monitor for months not included in this modeling (i.e., February, March, November, and 

December) while others do not. Seasonal relationships were developed between O3 response to 

emissions reductions and O3 concentration. Summer was the only season for which modeling 

data was created for all months (June, July, August). The winter relationships were developed 
4-41 

based on January modeling, the spring relationships were developed based on April/May 

modeling, and the autumn relationships were developed based on September/October modeling. 

The reduction in data points (31 or 61 instead of ~90) increases uncertainty in the statistical fit 

for these seasons. In addition, the modeling generally showed more O3 disbenefits to NOx

decreases in cooler months. So applying April/May relationships to March and 

September/October relationships to November could potentially underestimate O3 increases that 

would happen in those two months in the five urban study areas which measure O3 during March 

and/or November: Dallas, Denver, Houston, Los Angeles, and Sacramento. The eight months 

that were modeled capture a variety of meteorological conditions. Applying these 2007 

sensitivities to other years with potentially different meteorology and emissions adds uncertainty 

to the relationship between O3 response and O3 concentrations. Finally, if emissions change 

drastically between the modeled period and the time of the ambient data measurements this could 

also change the relationship between O3 response and O3 concentrations. The regressions derived 

from the 2007 modeling period are only applied to measurements made within 3 years of the 

modeled time period. Although some emissions changes did occur over this time period, we 

believe it is still reasonable to apply 2007 modeling to this relatively small window of 

measurements which occurs before and after the modeling. 

O3 response is modeled for across-the-board reductions in U.S. anthropogenic NOx (and 

VOC). These across-the-board cuts do not reflect actual emissions control strategies. The form, 

locations, and timing of emissions reductions that would be undertaken to meet various levels of 

the O3 standard are unknown. The across-the-board emissions reductions bring levels down 

uniformly across time and space to show how O3 would respond to changes in ambient levels of 

precursor species but do not reflect spatial and temporal heterogeneity that may occur in local 

and regional emissions reductions. In cases where VOC reductions were modeled, equal 

percentage NOx and VOC reductions were applied in the adjustment methodology. Regional 

NOx reductions are likely to be the primary means used to reduce high O3 concentrations at DV 

monitors. In limited cases, VOC emissions reductions may also help lower high O3

concentrations at these locations. In actual control strategies, NOx and VOC reductions may be 

applied in combination but are unlikely to be applied in equal percentages. The available 

modeling constrained the NOx/VOC case to this type of control scenario. The across-the-board 

cuts and the equal percentage NOx and VOC reductions scenario does not optimize the lowest 

cost or least total emissions combinations as state and local agencies will likely attempt to 

achieve.
4-42 

Table 4-7. Summary of Qualitative Uncertainty Analysis of Key Air Quality Elements in the O3 NAAQS R

Source Description 

Potential influence of uncertainty on risk estimates 

KnowledgeBase uncertainty* 

Comments (KB: knowledge ba

Direction Magnitude uncertainty on risk estimates) 

A. O3 measurements 

Ozone concentrations measured by ambient monitoring instruments have inherent uncertainties associated with them. Additional uncertainties due to other factors may include: 

- monitoring network 

locations 

- Ozone monitoring 

seasons 

- monitor 

malfunctions 

- wildfire and smoke 

impacts 

- interpolation of 

missing data 

Both Low Low 

KB: Ozone measurements are as1⁄2 of the instrument’s Method Deppb for most instruments. EPA reassurance checks are performed data reported to AQS are certifieand the corresponding EPA regioKB: Monitor malfunctions sometimissing data or poor data qualitymalfunctions are usually flagged removed from AQS. In addition, trun several routines to identify suremoval. KB: There is a known tendency fwildfires to cause interference in 

collected by O3 analyzers were r

5.1–6.6 ppb per 100 μg/m3 of PM2007). However, smoke concentsignificant interferences are infrebelieved to be minimal. KB: Missing intervals of 1 or 2 howere interpolated, which may caHowever, due to the short length and the tendency for these perio

concentrations are low, the overaminimal. INF: EPA’s current O3 monitoring 

urban focus. Rural areas where O

tend to be under-represented by The network requirements also swithin each urban area must be s

concentrations in that area, whichigher measured concentrationsINF: Each state has a required Ovaries in length from May – Sept
4-43 

Source Description 

Potential influence of uncertainty on risk estimates 

KnowledgeBase uncertainty* 

Comments (KB: knowledge ba

Direction Magnitude uncertainty on risk estimates) 

states turn their O3 monitors off d

required season, while others leadiscrepancies in the amount of dmonths outside of the required mestimates attempt to minimize thmonths where O3 monitoring is re

B. Voronoi Neighbor Averaging (VNA) spatial fields 

VNA is a spatial interpolation technique used to estimate O3

concentrations in unmonitored areas, which has inherent uncertainty 

Both Low-Medium Low-Medium 

KB: VNA interpolates monitored 

provide estimates of O3 exposure 

urban areas. The VNA estimates distance from neighboring monitouncertainty tends to increase witsites. KB: The 15 urban areas each hanetworks which were generally sgradients in O3 concentrations. T

the VNA fields instead of daily or to reduce uncertainty by better cadiurnal patterns between O3 mon

C.CMAQ modeling 

Model predictions from CMAQ, like all deterministic photochemical models, have both parametric and structural uncertainty associated with them 

Both Medium Medium 

KB: Structural uncertainties are urepresentation of physical and chThese include: choice of chemicacharacterize reactions in the atmmodel and choice of planetary boKB: Parametric uncertainties inclinputs (hourly meteorological fielemissions, initial conditions, and KB: Uncertainties due to initial coa 10 day ramp-up period from whKB: Evaluations of models again

concentrations build confidence treasonable accuracy despite the comprehensive model evaluation shows generally acceptable modequivalent or better than typical smodeling simulations as summarHowever, both under-estimations at some times and locations. Ge
4-44 

Source Description 

Potential influence of uncertainty on risk estimates 

KnowledgeBase uncertainty* 

Comments (KB: knowledge ba

Direction Magnitude uncertainty on risk estimates) 

occur on low O3 days during the model did not fully capture rare woccurring in the Western U.S. 

D. Higher Order Decoupled Direct Method (HDDM) 

HDDM allows for the approximation of O3

concentrations under alternate emissions scenarios without re-running the model simulation multiple times using different emissions inputs. This approximation becomes less accurate for larger emissions perturbations especially under nonlinear chemistry conditions. 

Both Medium Medium 

KB: To accommodate increasing perturbations, the HDDM modelidistinct emissions levels to allow O3 response over the entire rang

replication of brute force hourly O

by the HDDM approximation was NOx cut conditions for each urba

Appendix 4D). At 50% NOx cut c

information from these multiple s

concentrations with a mean bias 1 ppb in all urban study areas cosimulations. At 90% NOx cut con

information from these multiple s

concentrations with a mean bias error less than +/- 4 ppb in all urb

E. Application of HDDM sensitivities to ambient data 

In order to apply 

modeled sensitivities to ambient measurements, regressions were developed which relate O3 response to 

emissions perturbations with ambient O3 concentrations for 

every season, hour-of-the-day and monitor location. Applying O3 responses based on this 

relationship adds uncertainty. 

Both Medium Medium 

KB: Preliminary work showed thawith these regressions were genmost season, hour-of-the-day, ancombinations for 2005 modeling Statistical significance was not ethis analysis since there were ov(322 monitors × 5 sensitivity coefseasons × 24 hours = 463,680 re

can quantify the goodness of fit fHowever it is not possible to quamodeled relationship to the actuaKB: The regression model providestimate and a standard error es

measured hourly O3 concentratio

central tendency which will inhervariability in O3 response. The st

coefficient was propagated throuhourly and daily maximum 8-hr a

various standard levels. These suncertainty associated with estimSince emissions reductions increthe standard errors were larger fo
4-45 

Source Description 

Potential influence of uncertainty on risk estimates 

KnowledgeBase uncertainty* 

Comments (KB: knowledge ba

Direction Magnitude uncertainty on risk estimates) 

standards. Mean (95th percentile

the 75 ppb adjustment case rang(2.87) ppb in the 15 urban study 

standard errors in hourly O3 for th

ranged from 0.54 (1.07) to 1.39 (errors occurred in Los Angeles a

F. Applying modeled sensitivities to unmodeled time periods 

Relationships between O3response and hourly O3concentration were developed based on 8 months of modeling: January and AprilOctober 2007. These relationships were applied to ambient data from 2006-2010. Some locations monitor for months not included in this modeling (February, March, November, and December) while others do not. 

Both Medium Medium 

KB: The eight months that were meteorological and emissions cosensitivities to other years with p

and emissions adds uncertainty t

response and O3 concentrations

the 2007 modeling period are onmade within 3 years of the modeemissions changes did occur oveis still reasonable to apply 2007 mwindow of measurements which modeling. INF: Seasonal relationships were 

response to emissions reduction

Summer was the only season for created for all months (June, Julyrelationships were developed baspring relationships were developmodeling, and the autumn relatioon September/October modeling(31 or 61 instead of ~90) increasfit for these months. In addition, tmore O3 disbenefits to NOx decre

applying April/May relationships September/October relationships underestimate O3 increases that 

months in the five urban study ar

March and/or November: Dallas, and Sacramento. 

G. Assumptions of across-the-board emissions reductions 

Ozone response is modeled for across-the-board reductions in U.S. anthropogenic NOx (and VOC). 

Both Low-Medium Low-Medium 

KB: The form, locations, and timiwould be undertaken to meet varare unknown. The across-the-bolevels down uniformly across tim
4-46 

Source Description 

Potential influence of uncertainty on risk estimates 

KnowledgeBase uncertainty* 

Comments (KB: knowledge ba

Direction Magnitude uncertainty on risk estimates) 

These across-the-board cuts do not reflect actual emissions control strategies. 

would respond to changes in ambut do not reflect spatial and temoccur in local and regional emiss

H. Assumption of equal percentage NOx and VOC 

reductions 

In cases where VOC reductions were modeled, equal percentage NOx and 

VOC reductions were applied in the adjustment methodology. 

Both Low-Medium Medium 

KB: NOx reductions are likely to b

reduce high O3 concentrations at 

VOC emissions reductions may a

concentrations at these locations

be applied in combination but are percentages. The available mode

case to this unrealistic scenario. 

VOC reductions scenario does nleast total emissions combinationwill likely attempt to achieve. 

I. Downscaler 

Downscaler combines monitored and modeled concentrations to produce a “fused” air quality surface. Uncertainties may occur in sparsely monitored regions, or in urban areas with dense monitoring networks and large spatial gradients. 

Both Low-Medium Low-Medium 

KB: Downscaler combines modeconcentrations to provide estima

unmonitored areas while correctiThe cross-validation analysis in ADownscaler generally gives more quality in monitored locations thamodeled values alone. However, uncertainty associated with the elocations. KB: The air quality surfaces modnational-scale risk assessment wconcentrations, which tend to haother metrics such as peak concuncertainty. INF: The cross-validation analysthat Downscaler tends to over-esunder-estimate high concentratioestimates in monitored locations locations are often chosen to capthus there might be some bias tounmonitored areas. 
4-47 

4.6 REFERENCES 

Abt Associates, Inc. 2010a. Environmental Benefits and Mapping Program (Version 4.0). 

Bethesda, MD. Prepared for U.S. Environmental Protection Agency Office of Air Quality 

Planning and Standards. Research Triangle Park, NC. <http://www.epa.gov/air/benmap>. 

Abt Associates, Inc. 2010b. Model Attainment Test Software (Version 2). Bethesda, MD. 

Prepared for the U.S. Environmental Protection Agency Office of Air Quality Planning 

and Standards. Research Triangle Park, NC. 

<http://www.epa.gov/scram001/modelingapps.mats.htm.> 

Bell, M.L.; A. McDermott; S.L. Zeger; J.M. Samet and F. Dominici. 2004. Ozone and short-term 

mortality in 95 U.S. urban communities, 1987-2000. JAMA. 292:2372-2378. 

Berrocal, V.J.; A.E. Gelfand and D.M. Holland. 2012. Space-time data fusion under error in 

computer model output: an application to modeling air quality. Biometrics. 68(3):837-

848. 

Chen, J.R.; Zhao; Z. Li. 2004. Voronoi-based k-order neighbor relations for spatial analysis. 

ISPRS J Photogrammetry Remote Sensing. 59(1-2):60-72. 

Duff, M.; R. L. Horst; T.R. Johnson, 1998. Quadratic Rollback: A Technique to Model Ambient 

Concentrations Due to Undefined Emission Controls. San Diego, CA: Presented at the 

Air and Waste Management Annual Meeting, June 14-18, 1998. 

Fann, N.; A.D. Lamson; S.C. Anenberg; K. Wesson; D. Risley; B.J. Hubbell. 2012. Estimating 

the national public health burden associated with exposure to ambient PM2.5 and ozone. 

Risk Analysis. 32:81-95. 

Gold, C. 1997. Voronoi Methods in GIS, Vol. 1340. In Algorithmic Foundation of Geographic 

Information Systems (Kereveld M., J. Nievergelt, T. Roos, P. Widmayer, eds.). Lecture 

notes in Computer Science, Berlin: Springer-Verlag, 21-35. 

Hall, E.; A. Eyth; S. Phillips. 2012. Hierarchical Bayesian Model (HBM)-Derived Estimates of 

Air Quality for 2007: Annual Report. (EPA document number EPA/600/R-12/538). 

< http://www.epa.gov/heasd/sources/projects/CDC/AnnualReports/2007_HBM.pdf>. 

Jerrett, M.; R.T. Burnett; C.A. Pope, III; K. Ito; G. Thurston; D. Krewski; Y. Shi, E. Calle and 

M. Thun. 2009. Long-term ozone exposure and mortality. New England Journal of 

Medicine. 360:1085-1095. 

Johnson, T. 2002. A Guide to Selected Algorithms, Distributions, and Databases Used in 

Exposure Models Developed by the Office of Air Quality Planning and Standards. 

Prepared by TRJ Environmental, Inc. for the U.S. Environmental Protection Agency. 

Research Triangle Park, NC: Office of Research and Development. 

National Research Council of the National Academies. 2008. Estimating Mortality Risk 

Reduction and Economic Benefits from Controlling Ozone Air Pollution. Washington, 

DC: The National Academies Press. 

Rizzo, M. 2005. A Comparison of Different Rollback Methodologies Applied to Ozone 

Concentrations. Posted on November 7, 2005. 

<http://www.epa.gov/ttn/naaqs/standards/ozone/s_O3_cr_td.html.> 
4-48 

Rizzo, M. 2006. A Distributional Comparison between Different Rollback Methodologies 

Applied to Ambient Ozone Concentrations. Posted on May 31, 2006. 

<http://www.epa.gov/ttn/naaqs/standards/ozone/s_O3_cr_td.html.> 

Simon, H.; K. Baker; N. Possiel; F. Akhtar; S. Napelenok; B. Timin; B. Wells. 2012. Modelbased Rollback Using the Higher Order Direct Decoupled Method (HDDM). 

<http://www.epa.gov/ttn/naaqs/standards/ozone/s_O3_td.html>. 

Simon, H.; K. R. Baker; F. Akhtar; S.L. Napelenok; N. Possiel; B. Wells and B. Timin. 2013. A 

direct sensitivity approach to predict hourly ozone resulting from compliance with the 

National Ambient Air Quality Standard. Environmental Science and Technology. 

47:2304-2313. 

Smith, R.L., B. Xu, P. Switzer. 2009b. Reassessing the relationship between ozone and shortterm mortality in U.S. urban communities. Inhale Toxicol. 21:37-61. 

Timin, B.; K. Wesson and J. Thurman. 2010. Application of Model and Ambient Data Fusion 

Techniques to Predict Current and Future Year PM2.5 Concentrations in Unmonitored 

Areas, in D.G. Steyn and S.T. Rao (eds.), Air Pollution Modeling and Its Application XX,

Netherlands: Springer, pp. 175-179. 

U.S. Environmental Protection Agency. 2007. Review of the National Ambient Air Quality 

Standards for Ozone: Policy Assessment of Scientific and Technical Information OAQPS 

Staff Paper. Washington, DC: EPA Office of Air and Radiation. (EPA document number 

U. S. EPA. 2012a. Integrated Science Assessment for Ozone and Related Photochemical 

Oxidants: Third External Review Draft. Research Triangle Park, NC: EPA Office of Air 

Quality Planning and Standards. (EPA document number EPA-452/R-07-007; 

EPA/600/R-10/076C). 

U.S. EPA. 2012b. Total Risk Integrated Methodology (TRIM) - Air Pollutants Exposure Model 

Documentation (TRIM.Expo / APEX, Version 4.4) Volume I: User’s Guide. Research 

Triangle Park, NC: Office of Air Quality Planning and Standards. (EPA document 

number EPA-452/B-12-001a). <http://www.epa.gov/ttn/fera/human_apex.html>. 

U.S. EPA. 2012c. Total Risk Integrated Methodology (TRIM) - Air Pollutants Exposure Model 

Documentation (TRIM.Expo / APEX, Version 4.4) Volume II: Technical Support 

Document. Research Triangle Park, NC: Office of Air Quality Planning and Standards. 

(EPA document number EPA-452/B-12-001b). 

<http://www.epa.gov/ttn/fera/human_apex.html>. 

Wells, B.; K. Wesson and S. Jenkins. 2012. Analysis of Recent U.S. Ozone Air Quality Data to 

Support the O3 NAAQS Review and Quadratic Rollback Simulations to Support the First 

Draft of the Risk and Exposure Assessment. 

<http://www.epa.gov/ttn/naaqs/standards/ozone/s_O3_td.html>. 

Zhang, L.; D.J. Jacob; N.V. Smith-Downey; D.A. Wood; D. Blewitt; C.C. Carouge; A. van 

Donkelaar; D.B.A. Jones; L.T. Murray and Y. Wang. 2011. Improved estimate of the 

policy-relevant background ozone in the United States using the GEOS-Chem Global 

Model with 1/2°x2/3° horizontal resolution over North America." Atmospheric 

Environment. 45:6769-6776. 

Zanobetti, A. and J. Schwartz. 2008. Mortality displacement in the association of ozone with 

mortality: an analysis of 48 cities in the United States. American Journal of Respiratory 

and Critical Care Medicine. 177:184-189.
5-1 

5 CHARACTERIZATION OF URBAN-SCALE HUMAN EXPOSURE 

As part of the previous 2007 ozone (O3) NAAQS review, EPA staff conducted exposure 

analyses for the general population, all school-age children (ages 5-18), all active school-age 

children,1 and asthmatic school-age children (U.S. EPA, 2007a,b). Population-based exposures 

were simulated for these study groups residing in 12 urban study areas2

 considering recent years 

of air quality and for just meeting the existing 8-hour (8-hr) standard and several potential 

alternative 8-hr standards. In each of these 12 urban study areas, estimated daily maximum 8-hr 

average O3 exposures concomitant with moderate or greater exertion levels were compared with 

benchmark exposures concentrations, i.e., concentration levels at which adverse health responses 

were observed in controlled human exposure studies while exercising. EPA also estimated risk of 

impaired lung function for two study groups – all school-age children and asthmatic school-age 

children – in these same 12 study areas using exposure-response (E-R) relationships developed 

from controlled human exposure studies combined with the population-based exposures. 

The exposure analysis conducted for this current NAAQS review builds upon the 

methodology and lessons learned from the exposure analyses conducted in previous O3 reviews 

(U.S. EPA, 1996a, 2007a,b) and information provided in the O3 ISA (U.S. EPA, 2013). Here, we 

estimate exposures for people residing in 15 urban study areas in the U.S.3 The population-based 

exposures to ambient O3 concentrations were modeled using EPA’s Air Pollutants Exposure 

(APEX) (US EPA, 2012a,b). Exposures were calculated considering ambient O3 concentrations 

in recent years, using 2006 to 2010 spatially interpolated ambient monitoring data. Exposures 

were also estimated considering alternative air quality scenarios, that is, where O3 concentrations 

just meet the existing 8-hr O3 NAAQS and at several other standard levels considering the same 

indicator, form, and averaging time, based on adjusting data as described in Chapter 4. 

Exposures were modeled for (1) all school-age children (ages 5-18), (2) asthmatic school-age 

children (ages 5-18), (3) asthmatic adults (ages 19-95), and (4) all older adults (ages 65-95), each 

 

1

 In the previous 2007 exposure assessment, a study group of active school-age children was identified as children 

having their median daily physical activity index (PAI) over the exposure period ≥ 1.75, an activity level 

characterized by exercise physiologists as being “moderately active” or “active” (McCurdy, 2000). 2 The twelve study areas evaluated in the 2007 exposure assessment were Atlanta, Boston, Chicago, Cleveland, 

Detroit, Houston, Los Angeles, New York, Philadelphia, Sacramento, St. Louis, Washington D.C. (an area which 

at that time was modeled to include Baltimore as part of the Baltimore-Northern Virginia MSA). 3

 In addition to the twelve study areas identified in the 2007 exposure assessment, staff has added Dallas and 

Denver, while also separately modeling Baltimore (from Washington D.C.) in this current assessment. Inclusion 

of Seattle, WA was considered but not included due to a lack of appropriate monitoring data. 
5-2 

while at moderate or greater exertion level at the time of exposure.4 The strong emphasis on 

children, asthmatics, and older adults reflects the finding of the last O3 NAAQS review (U.S. 

EPA, 2007a) and the O3 ISA (U.S. EPA, 2013, Chapter 8) that these are important at-risk groups. 

As was done in the previous review, estimated daily maximum 8-hr average exposures are 

compared with exposure benchmark levels based on adverse health effects observed in controlled 

human exposure studies. Specific exposure model output of interest for this HREA chapter are 

the percent (and number) of people exposed one time (or multiple occurrences) at or above these 

8-hr average O3 concentrations of concern, all while at moderate or greater exertion levels. These 

exposure modeling results provide context on exposure across each of the urban study areas 

given the existing and alternative ambient air quality standard scenarios (i.e., who is likely 

exposed, how many in people in the exposure study group of interest, how often per year, etc.) 

though not directly providing an estimate of human health risk per se. However, the complete 

time series of individual exposures estimated by APEX in this assessment (not simply the daily 

maximum 8-hr average concentrations) then serve as input to a lung function risk module that 

estimates health risk based on information developed from controlled human exposure studies 

(Chapter 6). 

This chapter first provides a brief overview of human exposure and exposure modeling 

using APEX (section 5.1), the scope of this O3 exposure assessment and key inputs used to 

model exposure in the 15 U.S. study areas selected (section 5.2), and followed by the main body 

exposure results (section 5.3). Then, section 5.4 presents an assemblage of targeted analyses 

designed to provide additional insight to the main body of exposure results by focusing on 

important data inputs, additional at-risk populations, lifestages, or scenarios, influential attributes 

in estimating exposures, and performance evaluations. The results of these and other exposure 

model targeted analyses are integrated in a variability and uncertainty characterization section 

(section 5.5) along with a final section summarizing the key observations for this chapter 

(section 5.6). 

5.1 SYNOPSIS OF OZONE EXPOSURE AND EXPOSURE MODELING 

5.1.1 Human Exposure 

Human exposure to a contaminant is defined as “contact at a boundary between a human 

and the environment at a specific contaminant concentration for a specific interval of time,” and 

 

4

 The “all school-age children” study group includes both asthmatic and non-asthmatic children ages 5 to 18. The 

“all older adults” includes both asthmatic and non-asthmatic older adults ages 65 to 95. Note also that the 8-hr 

average exposure of interest in both this and the previous assessment was concomitant with moderate or greater 

exertion for all study groups. 
5-3 

has units of concentration times duration (National Research Council, 1991). For air pollutants 

the contact boundary is nasal and oral openings in the body, and personal exposure of an 

individual to a chemical in the air for a discrete time period is fundamentally quantified as (Lioy, 

1990; National Research Council, 1991): 

 Equation (5-1) 

where E[t1,t2] is the personal exposure or exposure concentration during the time period 

from t1 to t2, and C(t) is the concentration at time t in the breathing zone. The breathing rate at 

the time of exposure will influence the dose received by the individual. While we do not directly 

estimate dose in this assessment, intake is the total O3 inhaled (i.e., exposure concentration, 

duration, and ventilation combined).5

5.1.2 Estimating Ozone Exposure 

Exposure to O3 can be directly estimated by monitoring the concentration of O3 in a 

person’s breathing zone (close to the nose/mouth) using a personal exposure monitor. Studies 

employing this measurement approach have been reviewed in the O3 ISA and EPA O3 Air 

Quality Criteria Documents (U.S. EPA, 1986, 1996b, 2006, 2013). Personal exposure 

measurements from these studies are useful in describing a general range of exposure 

concentrations (among other reported measurement data) and in identifying factors that may 

influence varying exposure levels. However, these measurement studies are largely limited by 

the disparity between sample measurement duration and exposure concentration averaging-times 

of interest and in appropriately capturing variability in population exposure occurring over large 

geographic areas , particularly when considering both concentration (e.g., spatial variability) and 

population (e.g., age, sex) attributes that influence exposure. 

Ozone exposure for individuals, small groups of individuals or large populations can be 

calculated indirectly (or modeled) using Equation (5-1). When employing such an approach in a 

population-based exposure assessment, two basic types of input data are needed; a time-series of 

O3 concentrations that appropriately represents spatial heterogeneity in O3 concentrations and a 

corresponding time-series of locations visited by the people exposed. When considering air 

pollutant concentrations, population exposure models are commonly driven by ambient 

concentrations. These ambient concentrations may be provided by monitoring data, by air quality 

model estimates, or perhaps by a combination of these two data sources. Then, an understanding 

 

5

 In Chapter 6, the estimation of risk combines the time series of both the personal exposure concentrations and 

ventilation rate, among other variables in essentially calculating a dose, though not explicitly output from the 

model. 

  2

1

[ , ] ( ) 1 2

t

t

E t t C t dt
5-4 

of the relationships between ambient pollutants and the locations people occupy is needed. This 

is because human exposure, regardless of the pollutant or whether one is interested in individual 

or population exposure, depends on where an individual is located, how long they occupy that 

location, and what the pollutant concentration at the point of contact is. Furthermore, if interested 

in air pollutant intake rate or dose, one needs to know what activity the person is performing 

while exposed. 

Thus, the types of measurement and modeling studies that provide information for more 

realistically estimating exposure to O3 can be augmented from the above list to include studies 

of: (1) O3 formation, deposition, and decay, (2) people’s locations visited and activities 

performed, (3) human physiology, and (4) local scale meteorological measurements and/or 

modeling. Useful data derived from these varied studies are O3 concentrations (i.e., fixed site, 

personal exposure, indoor and outdoor locations), built environment physical factors (i.e., air 

exchange rates (AERs), infiltration rates, decay and deposition rates), human time-locationactivity patterns (minute-by-minute, hourly, daily, and longer-term), time-averaged or activityspecific breathing rates among varying sexes and/or lifestages, and hourly ambient temperatures. 

When integrating these varied data (among others such as population demographics and 

disease prevalence) and understanding factors affecting exposure, exposure models can extend 

beyond the limited information given by measurement data alone. For example, an exposure 

model can reasonably estimate exposures for any perceivable at-risk population (e.g., asthmatics 

living in a large urban area) and considering any number of hypothetical air quality conditions 

(e.g., just meeting a daily maximum 8-hr average concentration of 70 ppb). Exposure models that 

account for variability in human physiology can also realistically estimate pollutant intake by 

using activity-specific ventilation rates. These types of measurements cannot realistically be 

performed for a study group or population of interest, particularly when considering time, cost, 

and other constraints. The following section provides an overview of how such exposure 

modeling can be done using APEX, the model developed by EPA to perform such calculations 

and used to estimate O3 exposures in this HREA. 

5.1.3 Modeling Ozone Exposure Using APEX 

EPA has developed the APEX model for estimating human population exposure to 

criteria and air toxic pollutants, used most recently in estimating exposures for the O3 (U.S. EPA, 

2007b), nitrogen dioxide (U.S. EPA, 2008), sulfur dioxide (U.S. EPA, 2009a), and carbon 

monoxide (U.S. EPA, 2010) NAAQS reviews. APEX is a probabilistic model designed to 

account for the numerous sources of variability that affect people’s exposures. An overview of 

the approaches used by APEX to estimate exposure concentrations is found in Appendix 5A with 

details provided in U.S. EPA (2012a,b). 
5-5 

Briefly, APEX simulates the movement of individuals through time and space and 

estimates their exposure to a given pollutant while occupying indoor, outdoor, and in-vehicle 

locations. The model stochastically generates simulated individuals in selected study areas using 

census-derived probability distributions for demographic characteristics. Population 

demographics are drawn from the 2000 Census data6

 at a tract level, and a national commuting 

database based on 2000 Census data provides home-to-work commuting flows between tracts.7

Any number of individuals can be simulated, and collectively they approximate a random 

sampling of people residing in a particular study area. 

Daily activity patterns for individuals in a study area, an input to APEX, are obtained 

from detailed daily time-location-activity pattern survey data that are compiled in the 

Consolidated Human Activity Database (CHAD) (McCurdy et al., 2000; U.S. EPA, 2002). These 

daily diaries are used to construct a sequence of locations visited and activities performed for 

APEX simulated individuals consistent with their demographic characteristics, day-type (e.g., 

weekend or weekday), and season of the year, as defined by ambient temperature regimes 

(Graham and McCurdy, 2004). The time-location-activity data input to APEX are linked with 

personal attributes of the surveyed individuals, such as age, sex, employment status, day-of-week 

surveyed, and daily maximum and daily mean temperature. These specific personal attribute data 

are then used by APEX to best match the daily diary with the simulated study group of interest, 

using the same variables as first-order diary selection characteristics. The approach is designed to 

capture the important attributes contributing to an individuals’ time-location-activity pattern, and 

of particular relevance here, time spent outdoors (Graham and McCurdy, 2004). In using a 

diverse collection of time-location-activity diaries that capture the duration and frequency of 

occurrence of visitations/activities performed, APEX can simulate expected variability in human 

behavior, both within and between individuals. This, combined with exposure concentrations, 

allows for the reasonable estimation of the magnitude, frequency, pattern, and duration of 

exposures an individual experiences. 

A key concept in modeling exposure using APEX is the microenvironment, a term that 

refers to the immediate surroundings of an individual at a particular time. APEX has a flexible 

approach for modeling micro-environmental concentrations whereas the model user defines the 

type, number and characteristics of the microenvironments to be modeled. Typical 

microenvironments include indoors at home, indoors at school, near roadways, inside cars, and 

outside home. In this exposure assessment, all microenvironmental O3 concentrations are derived 

from ambient O3 concentrations input to APEX and are estimated using either a mass-balance or 

 

6

 Due to resource limitations and data availability, the 2010 Census data were not processed in time for use in this 

HREA, except for a limited sensitivity evaluation performed in section 5.4.4. 7

 There are approximately 65,400 census tracts in the ~3,200 counties in the U.S. 
5-6 

transfer factors approach, selected by the user. The mass balance approach assumes that the air 

in an enclosed microenvironment is well-mixed and that the air concentration is spatially 

uniform at a given time within the microenvironment. The approach employs indoor-to-outdoor 

AERs (i.e., number of complete air exchanges per hour) and considers removal mechanisms such 

as deposition to building surfaces and chemical decay rates. The transfer factors model is simpler 

than the mass balance model, and employs two variables, a proximity factor, used to account for 

proximity of the microenvironment to sources or sinks of pollution, or other systematic 

differences between concentrations just outside the microenvironment and the ambient 

concentrations, and a penetration factor, which quantifies the degree to which the outdoor air 

penetrates into the microenvironment. 

Activity-specific simulated breathing rates of individuals are used in APEX to 

characterize intake received from an exposure. This is done because controlled human exposure 

studies have shown adverse health outcomes are associated with both elevated concentrations 

and study participant exertion levels. The breathing rates calculated by APEX are derived from 

the energy expenditure associated with each simulated individual’s activity performed, adjusted 

for age- and sex-specific physiological parameters (Graham and McCurdy, 2005). The energy 

expenditure estimates themselves are derived from distributions of METS8

 (or metabolic 

equivalents of work) associated with every activity performed (McCurdy et al., 2000, using 

Ainsworth et al., 1993). 

An important feature of APEX is the ability to account for variability in exposure by 

representing input variables as statistical distributions along with conditional variables, where 

appropriate. For example, the distribution of AERs in a home, office, or motor vehicle can 

depend on the type of heating and air conditioning present, which are also stochastic inputs to the 

model, as well as the ambient temperature on a given day. The user can choose to keep the value 

of a stochastic parameter constant for the entire simulation (appropriate for the volume of a 

house), or can specify that a new value shall be drawn hourly, daily, or seasonally from specified 

distributions. 

Finally, APEX calculates a unique time-series of exposure concentrations on the order of 

minutes or smallest diary event duration that each simulated individual may experience during 

the modeled time period, based on that individual’s estimated microenvironmental 

concentrations and the time spent in each of sequence of microenvironments visited according to 

the time-location-activity diary of each individual. Then, hourly average exposures of each 

 

8

 METS are a dimensionless ratio of the activity-specific energy expenditure rate to the basal or resting energy 

expenditure rate. The metric is used by exercise physiologists and clinical nutritionists to estimate work 

undertaken by individuals as they go through their daily activities (Montoye et al., 1996). 
5-7 

simulated individual are estimated using time-weighted averages of the within-hour exposures. 

From hourly exposures, APEX calculates other time averaged exposures of interest (e.g., 8-hr or 

daily average) that a simulated individual experiences during the modeled period. 

5.2 SCOPE OF THE EXPOSURE ASSESSMENT 

This section broadly presents the scope of the exposure assessment including descriptions 

of the modeling domains, ambient concentrations used, time periods and populations modeled, as 

well as identifying key approaches, inputs and outputs used by APEX in estimating population 

O3 exposures. Detailed descriptions regarding APEX modeling, model inputs and other 

supporting information are provided in Appendices 5A-E and the APEX user’s guide and 

technical support documents (U.S. EPA 2012a,b). Figure 5-1 illustrates the general conceptual 

framework for generating our population exposure concentrations, including the time-series of 

exposure and ventilation rate output generated for input to the lung function risk calculations in 

Chapter 6. 

5.2.1 Urban Areas Selected 

The selection of urban areas to include in the exposure assessment considered the 

location of O3 epidemiological studies, the availability of ambient O3 monitoring data, and the 

desire to represent a range of geographic areas, encompassing variability in climate and 

population demographics. Specifically, the criteria included the following: 

 The overall set of urban locations should represent a range of geographic areas, urban 

population demographics, and climate, beginning with study areas selected in the 2007 

O3 NAAQS review. 

 The locations should be focused on areas that do not meet or are close to not meeting the 

existing 8-hr O3 NAAQS and should include areas having O3 non-attainment 

designations. 

 There must be sufficient O3 ambient air quality data for the recent 2006-2010 period. 

 The study areas should include the 12 urban study areas modeled in the epidemiologicbased risk assessment (Chapter 7). 
5-8 

Figure 5-1. Conceptual Framework Used for Estimating Study Area Population O3 Exposure Concentrati
5-9 

Based on these selection criteria, we chose the 15 study areas listed in Table 5-1 to 

develop our population exposure estimates. We then defined an air quality domain for each 

study area, broadly bounding the ambient concentration field where exposures were to be 

estimated. To do this, we evaluated (1) counties modeled in the previous 2007 O3 NAAQS 

review common to current study areas, (2) political/statistical county aggregations (e.g., whether 

in a metropolitan statistical areas or MSAs), and (3) if the study area was designated as a nonattainment area (NAA), the counties that were part of the NAA list. We identified a final list of 

215 counties9

 to comprise the air quality domain for the 15 study areas, the names of which are 

provided in Appendix 5B. 

5.2.2 Time Periods Simulated 

The exposure periods modeled are the O3 seasons for which routine hourly O3 monitoring 

data were available for years 2006 to 2010 (Table 5-1), and defined by 40 CFR part 58, 

Appendix D, Table D-3. These periods are designed to reasonably capture year-to-year 

variability in ambient concentrations and meteorology and include most of the high 

concentration events occurring in each area. Having this wide range of air quality data across 

multiple years allows us to more realistically estimate a range of exposures, rather than using a 

single year of air quality data. While the number of O3 monitors in operation may vary slightly 

from year to year, we assumed consistent representation by the complete set of all monitors 

within a study area. Thus the spatial representation of each study area using the statistically 

interpolated data remained consistent for each year over the simulation period (see section 5.2.3). 

5.2.3 Ambient Concentrations Used 

We used the available hourly ambient monitor concentration data within and around each 

study area along with a statistical interpolation technique (Chapter 4) to estimate hourly census 

tract concentrations within the counties comprising each study area. These concentrations served 

as the ‘base’ air quality input for each study area year. Ambient concentrations were also 

adjusted to just meet the existing standard (75 ppb, 4th highest 8-hr average, averaged over a 3-

year period) and alternative standard levels (70, 65, 60, and 55 ppb) using an air quality model 

and the statistical interpolation technique (Chapter 4). 

These estimated hourly census tract O3 concentrations served as the APEX air districts, 

the basic ambient concentrations from which each simulated individual’s microenvironmental 

concentrations are estimated. Having these temporally and spatially resolved air districts in each 

study area allows for better utilization of APEX spatial and temporal capabilities in estimating 

 

9

 Of the 215 counties defining the air quality domain, 207 remained in the exposure model domain. 
5-10 

exposure. Because APEX simulates where individuals are located at specific times of the day, 

more realistic exposure estimates are obtained in simulating the contact of individuals with these 

spatially and temporally diverse concentrations. 

Table 5-1. General Characteristics of the Population Exposure Modeling Domain 

Comprising Each Study Area. 

Study Area 

(Abbreviation) O3 Season1

Study Area Number of: 

Counties

Ambient 

Monitors

APEX Air 

Districts

US Census 

Tracts 

People 

All School 

Age 

Children 

(age 5-18) 

All Ages 

(age 5-95)

Atlanta (ATL) Mar 1-Oct 31 32 14 664 678 860,649 3,850,951

Baltimore (BAL) Apr 1-Oct 31 7 12 603 618 505,140 2,209,226

Boston (BOS) Apr 1-Sep 30 7 13 1,005 1,028 905,208 4,449,291

Chicago (CHI) Apr 1-Oct 31 16 28 1,882 2,055 1,899,073 8,345,373

Cleveland (CLE) Apr 1-Oct 31 8 16 802 879 578,733 2,692,846

Dallas (DAL) Mar 1-Oct 31 11 21 1,012 1,036 1,097,004 4,698,392

Denver (DEN) Mar 1-Sep 30 12 25 655 675 560,137 2,626,239

Detroit (DET) Apr 1-Sep 30 9 13 1,419 1,454 1,016,896 4,572,479

Houston (HOU) Jan 1-Dec 31 10 19 779 802 970,528 3,925,054

Los Angeles (LA) Jan 1-Dec 31 5 50 2,000 3,352 3,620,972 14,950,340

New York (NY) Apr 1-Oct 31 27 32 1,900 4,889 3,843,450 18,520,868

Philadelphia (PHI) Apr 1-Oct 31 15 19 1,452 1,555 1,231,052 5,506,954

Sacramento (SAC) Jan 1-Dec 31 7 18 447 461 466,169 1,926,598

St. Louis (STL) Apr 1-Oct 31 15 16 494 518 527,755 2,340,325

Wash., DC (WAS) Apr 1-Oct 31 26 28 1,013 1,037 966,791 4,498,374

All Study Areas - 207 324 16,127 21,037 19,049,557 85,113,310

 

Even though we estimated O3 ambient concentrations occurring at all census tracts in 

each county-level study area using the combined ambient monitor data, VNA interpolation, and 

CMAQ-HDDM simulation approach, the urban study area exposure modeling domain was 

defined as a subset of these census tracts and were selected by using an overlay of the ambient 

monitor locations within the urban core of each study area’s air quality domain and a 30 km 

radius of influence. We used a 30 km zone of influence to remain consistent with what was done 

in the 1st draft O3 HREA, though in that exposure assessment, only the ambient monitoring data 

were used to represent the APEX air districts, hence concentrations measured at a particular 

monitoring site would be directly extrapolated outwards to all census tracts within 30 km of that 
5-11 

site. In contrast, by incorporating the VNA estimated concentrations at all census tracts and 

retaining the same 30 km radius of influence, we stress the significance of the monitor 

information in defining the urban core air quality while also reasonably estimating concentration 

gradients (where such gradients exist) with increasing distance from monitoring locations. 

Thus, all air districts10 and census tracts (and their spatially varying concentrations) that 

fall within the 30 km radius of each ambient monitor location were used to estimate the 

exposures, defining the final exposure modeling domain in each study area (Table 5-1). The 

monitor IDs used to select the census tracts to be modeled are provided in Appendix 5B, while 

the complete list of census tract IDs where exposures were modeled are within the APEX control 

files for each study area (and are the same for each simulation year). 

5.2.4 Meteorological Data Used 

APEX uses study area temperature data to select representative diaries for a particular 

day and in selecting an appropriate air exchange rate used to calculate indoor residential 

microenvironmental concentrations. APEX uses the data from the closest weather station to each 

Census tract. To ensure reasonable coverage for each study area, a few to several meteorological 

stations recording hourly surface temperature measurements were identified using data obtained 

from the National Weather Service ISH data files.11 Details regarding the meteorological stations 

selected and data processing are given in Appendix 5B, section 5B-8. Briefly, APEX requires the 

temperature input data to be 100% complete. In general, any missing values were filled using a 

linear interpolation or regression approach that employs information from proximal 

meteorological stations. Details regarding the number of missing values in any meteorological 

station by year are provided in Appendix 5B Table 5B-10. 

5.2.5 Populations Simulated 

Exposure was estimated for four at-risk study groups residing in each study area: all 

school-age children (ages 5-18), asthmatic school-age children, asthmatic adults (ages 19-95), 

and all older adults (ages 65-95). Due to the increased amount of time spent outdoors engaged in 

relatively high levels of physical activity (which increases intake), school-age children as a group 

are particularly at risk for experiencing O3-related health effects (U.S. EPA, 2013, Chapter 8). 

We report results for all school-age children down to age five, recognizing an increasing trend 

for younger children to attend school. Some U.S. states allow 4-year-olds to attend kindergarten, 

and most states have preschool programs for children younger than five. In 2000, six percent of 

 

10 The original number of air quality districts for New York and Los Angeles needed to be reduced by about half due 

to exceeding personal computer memory capacity when APEX used > 2,000 air districts. See Appendix 5B for 

details. 11 http://www.ncdc.noaa.gov/oa/climate/surfaceinventories.html 
5-12 

U.S. children ages 3 to 19 who attend school were younger than five years old (2000 Census 

Summary File 3, Table QT-P19: School Enrollment). Currently we do not estimate exposure for 

these younger children due to a lack of information that would let us confidently characterize 

these younger aged children. While EPA guidance recommends, for certain instances, an upper 

age group of children ages 16 through 21 (U.S. EPA, 2005), we restricted our upper age 

classification of children through age 18. In considering the expected variability in activity 

patterns over the span of ages 16 through 21 (e.g., time spent outdoors, time in school, each in 

contrast to time spent working) and the relatively small difference in respiratory physiology over 

that same age span compared with that of adults (e.g., Figure 5-22), factors critical for high O3

exposure and dose, we assumed simulated people age 19 to 21 would be best included in our 

adult study group. The number of people represented in each of the 15 study areas is given in 

Table 5-1 and, considering all study areas together, captures approximately 32.8 % of all 

children ages 5 to18 and 32.0 % of the total U.S. population ages 5 to 95. 

The number of asthmatic school-age children and asthmatic adults in each study area was 

estimated using asthma prevalence from the Center for Disease Control (CDC) and Prevention’s 

National Health Interview Survey (NHIS).12 Briefly, years 2006-2010 NHIS survey data were 

combined to calculate asthma prevalence, defined as the probability of a “Yes” response to the 

question: “do you still have asthma?” among those that responded “Yes” to the question “has a 

doctor ever diagnosed you with asthma?”. The asthma prevalence was first stratified by NHIS 

defined regions (Midwest, Northeast, South, and West), sex, age (single years for ages 0-17) or 

age groups (ages ≥ 18), and by a family income/poverty ratio.13 These new asthma prevalence 

estimates were then linked to U.S. census tract level poverty ratio probabilities (U.S. Census 

Bureau, 2007), also stratified by age and age groups, to generate a final database consisting of 

census tract level asthma prevalence for the entire U.S. A detailed description of how the data 

base was developed is presented in Appendix 5C, while the estimated asthma prevalence used 

for each census tract is provided in the APEX asthma prevalence input file. A summary of the 

asthma prevalence approximated for each urban study area, as weighted by the age, sex, and 

income/poverty level distributions comprising each urban study area, is provided here in Table 

5-2. 

All simulated individuals (either asthmatic or non-asthmatic) used time-location-activity 

data from CHAD, the most complete, high quality source of human activity data for use in 

exposure modeling. The current CHAD database contains over 53,000 individual daily diaries 

including time-location-activity patterns for individuals of both sexes across a wide range of ages 

 

12 See http://www.cdc.gov/nchs/nhis.htm (accessed October 4, 2011). 13 The income/poverty ratio threshold used was 1.5, that is the surveyed person’s family income was considered 

either ≤ or > than a factor of 1.5 of the U.S. Census estimate of poverty level for the given year. 
5-13 

(<1 to 94). The database is geographically diverse, containing activity pattern data from 

individuals residing in several major cities, suburban, and rural areas across the U.S. Time spent 

performing activities within particular locations can be on a minute-by minute basis, thus 

avoiding the smoothing of potential peak exposures longer event durations would yield. 

Table 5-3 summarizes the studies and number of diaries in CHAD used in this 

assessment, noting that the total CHAD diaries used by APEX is restricted to just over 41,000 

given our simulation age range (5-95) and additionally selected usability requirements.14 

Additional context regarding the representativeness of the CHAD data in estimating exposure is 

provided in section 5.3.1 and Appendix 5G. 

Table 5-2. Asthma Prevalence for Children and Adults Estimated by APEX in Each 

Simulated Study Area. 

Study Area 

Asthma Prevalence (%) 

Children (5-18) Adults (18-95) All People (5-95) 

Atlanta 9.6 6.5 7.2 

Baltimore 9.7 6.6 7.3 

Boston 11.4 7.9 8.6 

Chicago 10.7 7.8 8.4 

Cleveland 10.9 7.7 8.4 

Dallas 9.9 6.5 7.3 

Denver 8.9 7.7 7.9 

Detroit 11.1 7.7 8.5 

Houston 10.1 6.5 7.4 

Los Angeles 9.0 7.7 8.0 

New York 12.2 8.1 9.0 

Philadelphia 11.3 7.9 8.7 

Sacramento 9.0 7.8 8.1 

St. Louis 11 7.6 8.4 

Washington D.C. 9.5 6.4 7.1 

All Areas 10.5 7.6 8.2 

 

 

14 In this assessment, the CHAD diaries must be from persons having a known age, sex, day-of-week, and daily 

temperature. In addition, diaries must have no more than 3 hours total of missing location and/or activity data. 
5-14 

Table 5-3. Consolidated Human Activity Database (CHAD) Study Information and Diarydays Used by APEX. 

Activity Pattern Study 

(Abbrev.) 

General 

Study Area 

Study 

Years 

Subject

Ages 

Subjects 

(ages 4-94)

Diary-days 

(ages 4-94) 

Diary-days 

(ages 4-18)

Baltimore Retirement Home 

(BAL) 

Baltimore, 

MD 

1997-98 72 - 93 26 304 0

California Youth (CAY) California 1987-88 12 - 17 182 182 182

California Adults (CAA) California 1987-88 18 - 94 1,555 1,555 36

California Children (CAC) California 1989-90 <1 - 11 771 771 771

Cincinnati (CIN) Cincinnati, 

OH 

1985 <1 - 86 807 2,259 727

Detroit Exposure and 

Aerosol Research (DEA)1,2

Detroit, MI 2005-06 18 - 74 74 331 5

Denver CO Personal 

Exposure (DEN) 

Denver, CO 1982-83 18 - 70 410 714 7

EPA Longitudinal (EPA)1,2 RTP, NC 1999-2000, 

2002, 06-08

<1 - 60 10 1,386 0

LA Ozone Exposure: 

Elementary School (LAE) 

Los Angeles, 

CA 

1989 10 - 12 17 50 50

LA Ozone Exposure: High 

School (LAH) 

Los Angeles, 

CA 

1990 13 - 17 19 42 42

National Human Activity 

Pattern Study: Air (NHA) 

National 1992-94 <1 - 93 4,129 4,129 693

National Human Activity 

Pattern Study: Water 

(NHW) 

National 1992-94 <1 - 93 4,099 4,099 745

National-Scale Activity 

Survey (NSA) 

7 US metro. 

areas 

2009 35 - 92 1,192 6,825 0

Population Study of Income 

Dynamics I (ISR)1

National 1997 <1 - 13 1,904 3,507 3,507

Population Study of Income 

Dynamics II (ISR)1

National 2002-03 5 - 19 2,469 4,800 4,793

Population Study of Income 

Dynamics III (ISR)1,2

National 2007-08 10 - 19 1,351 2,619 2614

RTI Ozone Averting 

Behavior (OAB)1

35 US 

metro. areas

2002-03 2 - 12 575 2,187 2,187

RTP Panel (RTP)1 RTP, NC 2000-01 55 - 85 37 871 0

Seattle (SEA)1 Seattle, WA 1999-2002 6 - 91 178 1,624 317

Study of Use of Products 

and Exposure Related 

Behavior (SUP) 1,2

Sac/San 

Fran, CA 

Counties 

2006-10 1 - 88 696 2,533 994

Washington D.C. (WAS) Wash., DC 1982-83 18 - 71 686 686 10

Totals 1982 - 2010 <1 - 94 21,187 41,474 17,680

1

 Study data added after 2007 O3 NAAQS review. 

2

 Study data added after 2012 1st Draft O3 HREA. 
5-15 

APEX creates a sequence of daily diaries across the entire O3 season for each simulated 

individual using a method designed to capture the tendency of individuals to repeat activities, 

based on reproducing realistic variation in a key diary variable (Glen et al., 2008). For this O3

analysis, the key variable selected is the amount of time an individual spends outdoors each day, 

one of the most important determinants of exposure to high levels of O3 (see section 5.3.2). The 

longitudinal method targets two statistics, a population diversity statistic (D) and a within-person 

autocorrelation statistic (A). Values of 0.2 for D and 0.2 for A were initially developed based on 

analyses by Geyh et al. (2000) and Xue et al. (2004), with both studies evaluating groups of 

children ages 7 to 12 in a single study area. We adjusted values for D upwards to 0.5 to reflect a 

broader range of ages and to better estimate repeated activities.15 Further details regarding the 

development of the longitudinal methodology can be found in U.S. EPA (2012a, b). 

5.2.6 Key Physiological Processes and Personal Attributes Modeled 

The modeling of physiological processes relevant to the O3 exposure and intake is 

complex, particularly when representing inter- and intra-personal variability in energy 

expenditure (EE) and ventilation rates (VE). APEX has a module capable of estimating several 

variables associated with every activity performed by simulated individuals. Briefly, the module 

links the diary indicated activities to specific energy expended, the rate of oxygen consumed 

(VO2) and the associated ventilation rate, all considering the unique sequence of events 

individuals go through each simulated day. The activity-specific time-series of VE estimates 

ultimately serve as an important variable used in estimating O3 intake as well as in identifying 

when simulated individuals performing activities at moderate or greater exertion. In addition, 

age, sex, and body mass related physiological differences are specifically taken into account by 

the ventilation algorithm, derived using ventilation data obtained from several human studies 

(see Graham and McCurdy, 2005): 

E O b w V BM b b V BM b  age b sex  e  e  

2 3 2 0 1 ln( / ) ln( / ) ln (1 ) Equation (5-2) 

where, 

ln = natural logarithm of variable 

V E / BM 

 = activity specific ventilation rate, body mass normalized (L air/kg) 

bi = see Table 5-4 

 

15 A small D means that the overall variability between people in the key diary statistic is smaller than the variability 

observed over days within the same person. A D closer to 1 means that each person shows little variation over 

time relative to the variability between persons. 
5-16 

V O2 / BM 

 = activity specific oxygen consumption rate, body mass normalized (L 

O2/kg) 

age = age of the individual (years) 

sex = sex (-1 for males, +1 for females) 

eb = randomly sampled error term for between-person variability N{0, se}, 

(L air/kg) 

ew = randomly sampled error term for within-person variability N{0, se}, (L 

air/kg) 

As indicated by Equation (5-2), the random error (ε) is allocated to two variance 

components used to estimate the between-person (inter-individual variability) residuals 

distribution (eb) and within-person (intra-individual variability) residuals distribution (ew). The 

regression parameters b0, b1, b2, and b3 are assumed constant over time for all simulated 

individuals, eb is sampled once per person by APEX, whereas ew varies from event to event. 

Point estimates of the regression coefficients and standard errors of the residuals distributions are 

given in Table 5-4. See Appendix 5A, Isaacs et al. (2008), and Chapter 7 of the APEX TSD (US 

EPA, 2012b) for further discussion of this module. See also section 5.4.4 for a limited 

performance evaluation of this module in estimating ventilation rates. 

Table 5-4. Ventilation Equation Coefficient Estimates (bi) and Residuals Distributions (ei). 

Age 

group 

Ventilation Equation Coefficients1 Random Error1

b0 b1 b2 b3 eb ew

<20 4.3675 1.0751 -0.2714 0.0479 0.0955 0.1117

20-<34 3.7603 1.2491 0.1416 0.0533 0.1217 0.1296

34-<61 3.2440 1.1464 0.1856 0.0380 0.1260 0.1152

61+ 2.5826 1.0840 0.2766 -0.0208 0.1064 0.0676

1

 These are values of the coefficients and residuals distributions described by Equation (5-2) and described 

in Graham and McCurdy (2005).

Two key personal attributes determined for each simulated individual in this assessment 

are body mass (BM) and body surface area (BSA). Each simulated individual’s body mass is 

randomly sampled from age- and sex-specific body mass distributions generated from National 
5-17 

Health and Nutrition Examination Survey (NHANES) data for the years 1999-2004.16 Details in 

their development and the parameter values are provided by Isaacs and Smith (2005). Then ageand sex-specific body surface area can be estimated for each simulated individual based on 

logarithmic relationships developed by Burmaster (1998) using body mass as an independent 

variable as follows: 

2.2781 0.6821 BSA e BM   Equation (5-3) 

5.2.7 Microenvironments Modeled 

APEX is designed to estimate human exposure by using algorithms that attempt to 

capture the full range of O3 concentrations expected within several microenvironments. Broadly 

aggregated, these can be either indoor, inside a motor vehicle, near road, or outdoor locations. 

The two methods available in APEX for calculating pollutant concentrations within 

microenvironments are a mass balance model and a transfer factor approach. Table 5-5 lists the 

28 microenvironments selected for this analysis and the exposure calculation method used for 

each. Additional information on the linking of CHAD codes with APEX microenvironments can 

be found in Appendix 5B, section 5B-6. Further, information on what microenvironments were 

included as a location for each CHAD study is provided in Appendix 5B, Table 5B-2. 

The importance of modeling indoor microenvironments (e.g., homes, offices, schools) is 

underscored by research indicating that personal exposure measurements of O3 may not be wellcorrelated with ambient measurements and indoor concentrations are usually much lower than 

ambient concentrations (U.S. EPA, 2013, Section 4.3.3). We used mass balance modeling to 

estimate O3 concentrations in all indoor microenvironments, considering probabilistic 

distributions of temperature-dependent (where data were available) building air exchange and 

chemical decay rates. Parameter settings for each of these variables are provided in Appendix 

5B, while additional discussion regarding updates made to air exchange rates using more recent 

study data is given in Appendix 5E. 

The remaining microenvironments were modeled using a transfer factors approach. 

Outdoor microenvironmental concentrations were assumed equivalent to ambient concentrations, 

near-road concentrations were adjusted considering whether or not O3 concentrations were 

reduced by atmospheric reactions (e.g., scavenging by NOx) or other processes, and vehicular 

microenvironments considered both the outdoor concentration attenuation and 

 

16 Demographic (Demo) and body measurement (BMX) datasets for each of the NHANES studies were obtained 

from http://www.cdc.gov/nchs/nhanes/nhanes_questionnaires.htm. 
5-18 

infiltration/removal in the concentration estimation. Specific parameter settings for each of these 

variables are provided in Appendix 5B. 

Table 5-5. Microenvironments Modeled, Calculation Method Used, and Variables 

Included. 

Microenvironment 

Calculation 

Method Variables 

Indoor: Residence, Community Center or Auditorium, Restaurant, 

Hotel/Motel, Office building/Bank/Post Office, Bar/Night Club/Café, School, 

Shopping Mall/Non-Grocery Store, Grocery Store/Convenience Store, 

Metro-Subway-Train Station, Hospital/Medical/Care Facility, Industrial 

Factory/Warehouse, Other Indoor

Mass 

balance 

Building air 

exchange & 

chemical 

decay rates 

Outdoor: Residential, Park/Golf Course, Restaurant/Café, School 

Grounds, Boat, Other Outdoor Non-Residential

Factors None 

Near-road: Metro-Subway-Train Stop, Within 10 Yards of street, Parking 

Garage (covered or below ground), Parking lot (open)/Street parking, 

Service Station

Factors Proximity 

factors 

Vehicle: Cars/Light Duty Trucks, Heavy Duty Trucks, Bus, Train/Subway Factors Proximity & 

penetration 

factors 

5.2.8 Model Output 

APEX estimates the complete time series of exposure concentrations for every simulated 

individual and can summarize data using standardized time metrics (e.g., hourly or daily average, 

daily maximum 8-hr average) or can output the minute-by-minute exposure concentrations (as is 

needed for the risk estimation in Chapter 6). As an indicator of exposure to O3 air pollution, we 

selected the daily maximum 8-hr average O3 exposure17 for every simulated individual and 

stratified these exposures by exertion level at the time of exposure. This indicator was selected 

based on controlled human exposure studies where reported adverse health responses were 

associated with exposure to O3 and while the study subject was exercising.18 Factors important in 

calculating this indicator includes the magnitude, duration, frequency of exposures, and the 

breathing rate of individuals at the time of exposure. As a reminder, the calculated daily 

maximum 8-hr average exposure concentrations are distinct from that of daily maximum 8-hr 

average ambient concentrations by accounting for simulated individual’s time-location-activity 

patterns and O3 concentration decay/variation occurring within the occupied microenvironments. 

 

17 It is important to stress here that only the maximum 8-hr average O3 exposure concentration is retained for each 

day simulated, per person. While every day has twenty-four unique 8-hr averages and that it is entirely possible 

multiple benchmark exceedances could occur for an individual on certain high ambient O3 concentration days, 

staff judge this is not a practical output for the purposes of this assessment. 18 It is worth noting that the adverse health responses in the human clinical studies are generally based on 6.6 hour 

exposure to O3. Therefore, it is possible that the effects observed at benchmark levels identified using a 6.6 hour 

exposure could correspond to lower 8-hr exposures. 
5-19 

Benchmark levels used in this assessment include 8-hr average O3 exposure 

concentrations of 60, 70 and 80 ppb; the same benchmark levels used for the 2007 O3 exposure 

assessment (U.S. EPA, 2007b). Estimating exposures to ambient O3 concentrations at and above 

these benchmark levels is intended to provide perspective on the public health impacts of O3-

related health effects observed in human clinical and toxicological studies, but that cannot 

currently be evaluated in quantitative risk assessments (e.g., lung inflammation, increased airway 

responsiveness, and decreased resistance to infection). The 80 ppb benchmark level represents an 

exposure level where there is substantial clinical evidence demonstrating a range of O3-related 

effects including lung inflammation and airway responsiveness in healthy adults. The 70 ppb 

benchmark level reflects evidence that asthmatics have larger and more serious effects than 

healthy people as well as a substantial epidemiological evidence of adverse effects associated 

with O3 levels that extend below 80 ppb. The 60 ppb benchmark level represents the lowest 

exposure level at which O3-related effects have been observed in clinical studies of healthy 

individuals. See ISA section 6.2.1 for further discussions regarding the body of evidence 

supporting the selection of these benchmark levels. 

The level of exertion of achieved by all simulated individuals is approximated by an 

equivalent ventilation rate (EVR), that is, a time-averaged ventilation rate normalized by body 

surface area (BSA, in m2) and is calculated as VE/BSA, where VE is the ventilation rate in 

liters/minute. For identifying moderate or greater exertion occurring during any 8-hr average 

exposure period in this assessment, we used the lower bound EVR value of 13 (liters/min-m2

) 

based on a range of EVRs used by Whitfield et al. (1996) to categorize people engaged in 

moderate exertion activities for an 8-hr period. Whitfield et al. (1996) developed this range from 

EVR data reported in a 6.6-hr controlled human exposure study conducted by McDonnell et al. 

(1991), whereas, adult study participants were required to maintain a particular ventilation rate 

(generally between 35-45 L/minute) while exposed over the duration of the experiment. In 

APEX, EVR is calculated using an 8-hr averaging time as is done in calculating 8-hr exposures, 

though of interest in this exposure assessment are instances when the simulated individual 

experiences an 8-hr average exposure at or above the selected benchmark levels that 

simultaneously occurs while at a moderate or greater exertion level (i.e., 8-hr average EVR > 13 

L/min-m2

). 

APEX then calculates two general types of exposure estimates for the population of 

interest: the estimated number of people exposed to a specified O3 concentration level and, the 

number of days per O3 season that they are so exposed; the latter metric is expressed in terms of 

person-days. The former highlights the number of individuals exposed one or more times per O3

season at or above a selected benchmark level. The person-days measure estimates the number of 

times per season the simulated individuals are exposed at or above a selected benchmark level 
5-20 

and summed across individuals comprising the population. We note that a person-days metric 

conflates people and occurrences: one occurrence for each of 10 people would be counted the 

same as 10 occurrences for one person (i.e., 10 person-days at or above benchmark level). In this 

assessment we are more interested in reporting multiday exposures rather than total person-days, 

that is, the number of times an individual experiences multiple exposures at or above a 

benchmark level during an O3 season. Given the complexities of the exposure modeling, the four 

study groups considered, the 15 study areas, the 5 years of ambient air quality, the multiple air 

quality scenarios simulated, and ultimately the output data generated, including both single and 

multiday exposures for simulated individuals, the consolidation of the results and the related 

graphic depictions used in this assessment requires additional discussion. 

To begin, a simple example of exposure results is the estimated percent of asthmatic 

school-age children experiencing exposures at or above a single 8-hr benchmark level when 

considering air quality adjusted to just meet the existing 8-hr O3 standard (4th highest daily 

maximum 8-hr average O3 concentration averaged over a three year period) in Atlanta (Figure 5-

2). This presentation largely depicts the variability in O3 exposure across Atlanta during the five 

years of air quality evaluated (2006-2010, given by the x-axis) for each of the benchmark levels 

of interest. A general finding regarding temporal variability extracted from this graph would be 

that fewer asthmatic school-age children exceed daily maximum 8-hr average exposures of 60 

ppb (red symbol/lines) considering 2009 air quality adjusted to just meet the existing standard 

(the top panel heading of “75”) when compared with other simulation years (approximately 12% 

of asthmatic school-age children experienced such an exposure compared with upwards to 20%). 

Also worthy of mention is the two exposure results reported for year 2008 considering the 60 

ppb exposure benchmark of approximately 6% and 20%. Two values were generated for 2008 

due to the two 3-year averaging periods used to simulate just meeting the air quality standards 

(i.e., 2006-2008 and 2008-2010, respectively). The percent of study subjects exposed to higher 

benchmark levels is also presented in similar fashion (e.g., the percent of people experiencing 8-

hr exposures at or above 70 ppb is illustrated with a green symbol/line), though by definition, 

will always be at or below that estimated for the percent of people exceeding the 60 ppb 

benchmark in a given year. For example, only 5% of asthmatic school-age children are 

estimated to experience at least one daily maximum 8-hr exposure at or above 70 ppb 

considering 2006 air quality, while about 20% are estimated to exceed the 60 ppb benchmark 

level for that same year. Further, exposures at or above the highest exposure benchmark 

considered in this exposure assessment are indicated by a third colored symbol and continuous 

line (80 ppb, colored blue), and again by definition, the percent of study subjects exposed would 

be at or below that estimated for the 70 ppb exposure benchmark. 
5-21 

Figure 5-2. Percent of Asthmatic School-age Children in Atlanta with at least One Daily 

Maximum 8-hr Average O3 Exposure while at Moderate or Greater Exertion, 2006-2010 

Air Quality Adjusted to Just Meet the Existing Standard. This single panel display illustrates 

the exposure results by year (x-axes) including the two standard averaging periods (the sets of 

continuous lines each for 2006-2008 and 2008-2010), the three exposure benchmarks (60, 70, 80 

ppb - red, green, and blue lines) considering the adjusted air quality standard level (75 ppb, 

labelled top shaded area) in Atlanta (labelled right shaded area). 

Mindful of the further complexity when considering the four air quality standard 

scenarios (existing standard and three alternative standard levels) and 15 urban study areas, we 

elected to use a multi-panel graphing approach to succinctly summarize the exposure output data, 

while also retaining as much information as possible in a single page format to allow for visual 

analysis of trends and patterns. Figure 5-3 exhibits all of the dimensions of the exposure results 

mentioned above (i.e., year, benchmark level, and study area) along with distinguishing between 

the existing (75 ppb) and alternative standard levels (60, 65, 70 ppb). We elected to use the 

multi-panel display, going from left to right, to illustrate the impact to estimated exposures 

resulting from progressively increasing the stringency of the air quality standard. For example, 

the left most panel heading of “75” contains the exposure results when air quality was adjusted to 

just meet the existing 8-hr standard level of 75 ppb, i.e., the same results presented in Figure 5-2 

and described above. Also included in going to the right of this panel in Figure 5-3 are the 

exposure results considering a 70 ppb standard (panel heading of “70”), a 65 ppb standard (panel 

heading of “65”), and a 60 ppb standard (panel heading of “60”). 
5-22 

Figure 5-3. Percent of Asthmatic School-age Children in Atlanta with at least One Daily 

Maximum 8-hr Average O3 Exposure while at Moderate or Greater Exertion, 2006-2010 

Air Quality. This multi-panel display accounts for exposure results by year (x-axes), the three 

exposure benchmarks (60, 70, 80 ppb - red, green, and blue lines), and also includes exposure 

results considering four air quality standard levels (75, 70, 65, 60 ppb, panels left to right). 

Exposure results are then readily observed for any air quality scenario, year, or 

benchmark level of interest. For example, when considering the 70 ppb standard and 2006 

adjusted air quality, about 11% of asthmatic school-age children in Atlanta experience at least 

one daily maximum 8-hr average exposure of 60 ppb, while only about 5% experience exposures 

at or above the same benchmark level considering a 65 ppb standard also using 2006 adjusted air 

quality (Figure 5-3). In addition, fewer than 5% of asthmatic school-age children in Atlanta 

experience at least one benchmark exposure of 70 ppb considering any year and any air quality 

scenario, including just meeting the existing 75 ppb standard. These and other comparisons can 

be drawn from the presentation quite easily and, when including results for all 15 urban study 

areas in the figure, the variability in ambient concentrations and the impact of adjusting the air 

quality to just meet the standard levels of interest are also easily observed across the study areas. 

Because APEX simulates the complete time series of exposure for every simulated 

individual, also output is the number of times an individual experiences a benchmark exceedance 

over the duration of the simulation (i.e., the entire O3 season simulated in each study area). These 

data can be summarized in a similar multi-panel format as was described above, though differing 

slightly in composition from that shown in Figure 5-3. Instead of displaying the percent of 

people with at least one exceedance of each of the three benchmarks, presented are the percent of 

people with multiple exposures at or above a single benchmark within an O3 season. For 

example, Figure 5-4 illustrates the percent of asthmatic school-age children in Atlanta having 

more than one day where their daily maximum exposure was at or above 60 ppb (≥2, ≥4, and ≥6 

per O3 season), considering the 2006-2010 air quality adjusted to just meet the existing and 

alternative standards levels. When considering 2006 air quality adjusted to just meet the existing 

standard, approximately 10% of asthmatic school-age children experienced at least two days 

where their daily maximum 8-hr average exposure was at or above 60 ppb, though fewer than 
5-23 

5% experienced such exposures in 2009. When collectively considering all simulated air quality 

scenarios and years, fewer than 3% of asthmatic school-age children experienced at least four 

exposures at or above 60 ppb and virtually no asthmatic school-age children experienced six or 

more such exposures over the O3 season. 

Figure 5-4. Percent of Asthmatic School-age Children in Atlanta with Multiple (≥ 2, ≥ 4, ≥

6 per O3 season - red, green, and blue lines) Daily Maximum 8-hr Average O3 Exposures at 

or above 60 ppb while at Moderate or Greater Exertion, 2006-2010 Air Quality (x-axes) 

Adjusted to Just Meet 8-hr O3 Standard Levels of 75, 70, 65, 60 ppb (panels left to right). 

Also worth discussing is the appearance of a similar pattern between the benchmark level 

results (Figure 5-3) and the number of exceedances of a single benchmark (Figure 5-4). Because 

the ambient concentration is an important determinant in exposure concentrations, it is not 

surprising to see that the trend over years for people having at least one exposure at or above a 

particular benchmark level (e.g., 60 ppb) is similar to those experiencing at least two daily 

maximum 8-hr average exposures above 60 ppb (though a smaller percentage of the exposure 

study group). This is because years having the highest peak concentrations will yield the greatest 

percent of people above benchmark levels, and when one year has a day with the highest 

concentration, it is likely that year also has a second day with a similarly and relatively high 

concentration, and so on. Using the same logic, one might also conclude that there could be a 

pattern between the percent of people experiencing a single daily maximum 8-hr exposure of 70 

ppb and multiple exceedances (e.g., four) of 60 ppb also driven by the overall ambient 

concentration distribution. However, given that very few people experience multi-day 

benchmark exceedances, determining the relationship between the two (if present) may not be of 

practical significance. For brevity, the complete multiday exposure results for all APEX 

simulations are presented in Appendix 5F, with results presented for one study group (e.g., all 

school-age children) in the main body of this HREA. 
5-24 

5.3 EXPOSURE ASSESSMENT RESULTS 

5.3.1 Overview 

The results of the exposure analysis are presented as a series of figures focusing on the 

defined range of benchmark levels (i.e., people experiencing daily maximum 8-hr average O3

exposure concentrations ≥ 60, 70, and 80 ppb), noted as being of particular health concern 

(Section 5.2.8). A range of concentrations in the air quality data over the five year period (2006-

2010) were used in the exposure model, providing a range of estimated exposures output by 

APEX. The adjusted air quality was developed using two distinct 3-year period design values 

(2006-2008 and 2008-2010), as described in Chapter 4.19 Exposures were estimated for four 

study groups of interest (i.e., all school-age children (5-18), asthmatic school-age children, 

asthmatic adults (19-95), and older adults (65-95)) in each of the 15 study areas. 

In this exposure assessment, we are primarily interested in O3 exposures associated with 

the ambient air quality adjusted to just meet the existing and potential alternative O3 standards. 

Thus, most of the exposure results presented and discussed are for where ambient air quality was 

adjusted to just meet these particular scenarios. While understanding exposures and health risks 

associated with historical and existing air quality is important, the primary goal of this and any 

HREA is to evaluate to what extent the existing NAAQS, and its associated air quality, protect 

health and to what extent alternative NAAQS protect health. Exposure results associated with 

recent (base) air quality are briefly discussed here first, though largely reported in Appendix 5F. 

5.3.2 Exposure Modeling Results for Base Air Quality 

The exposure results for the base (unadjusted) air quality are distinguished from the other 

air quality scenario results primarily due to the wide ranging variability in estimated exposures 

across the study areas and years. The variability in exposures are the result of the wide ranging 

variability in ambient concentration levels, with some base year air quality in some study areas 

exhibiting air quality at or near that just meeting the existing 8-hr standard, while other study 

areas and years exhibiting base air quality levels much higher than the existing 8-hr standard. 

These exposures are informative in describing the existing or recent health risks associated with 

a unique air quality scenario, but because they variably diverge from a set concentration level of 

interest (such as the existing 8-hr standard), they are of limited relevance in evaluating the 

adequacy of either the existing NAAQS as well as potential alternative air quality standards. 

That said, detailed tabular and graphic presentations of exposure results associated with the base 

 

19 Thus, the year 2008 will have two sets of estimated exposures, one from each of the two sets of design values. 

Where mean results are presented in subsequent results sections, the two values given for year 2008 were first 

averaged to give a single exposure value for 2008 before averaging across all years. 
5-25 

air quality (years 2006-2010) are provided in Appendix 5F, with only key findings summarized 

in the following discussion. 

Consistent with observations regarding year-to-year variability in ambient concentrations 

(Chapter 4), most study areas have the greatest percent of all school-age children experiencing 

concentrations at or above the three benchmark levels during 2006 or 2007 along with having the 

lowest percent of all school-age children exposed during 2009 considering the base air quality. In 

general, between 20-40% of all school-age children experience at least one daily maximum 8-hr 

O3 exposure ≥ 60 ppb, 10-20% experience at least one O3 exposure ≥ 70 ppb, and 0-10% 

experience at least one O3 exposure ≥ 80 ppb, all while at moderate or greater exertion (i.e., an 8-

hr EVR ≥ 13 L/min-m2) and. Year-to-year variability and percent of study subjects exposed were 

similar for all school-age children and asthmatic school-age children, largely a function of 

having both simulated study groups using an identical activity diary pool to construct each 

simulated individual’s time series of activities performed and locations visited.20

The overall year-to-year pattern of exposure for asthmatic adults is similar to that 

observed for all school-age children, though the percent of the asthmatic adult study group 

exposed is lower by a factor of about three or more. Having a lower percent of asthmatic adults 

exposed is expected given that outdoor time expenditure is an important determinant of O3

exposure (section 5.4.2) and that adults spend less time outdoors than children (section 5.4.1), as 

well as adults having lower participation in outdoor events. The percent of all older adults 

experiencing exposures at or above the selected benchmark levels is lower by a fewer percentage 

points when compared with the results for asthmatic adults. Again, older adults, on average, 

would tend to spend less time outdoors and do so with less frequency when compared with both 

adults and children (section 5.4.1), in addition to fewer older adults performing activities at 

moderate or greater exertion for extended periods of time, thus leading to fewer people exposed 

to O3 concentrations of concern. 

The year-to-year patterns of the single and multiple exposure occurrences considering 

base air quality (2006-2010) were similar among the four exposure study groups, therefore only 

results for all school-age children will be summarized here. Depending on the year and study 

area, about 10-25% of all school-age children could experience at least two exposures above the 

60 ppb benchmark during the O3 season, while about 5-10% school-age children could 

experience at least four. Most study areas and years are estimated to have fewer than 5% of all 

school-age children experience six or more daily maximum 8-hr exposures ≥ 60 ppb considering 

the base air quality. When considering the multi-day exposures for all school-age children at or 

 

20 Using the same diary pool to simulate asthmatic and non-asthmatic children’s activity patterns is supported by 

similarities in time spent outdoors and exertion levels (HREA section 5.4.1.5). 
5-26 

above the 70 ppb benchmark, about 2-10% of all school-age children could experience at least 

two exposures during the O3 season, while experiencing four or more exposures were generally 

limited to fewer than 4% of all school-age children. Almost half of the study area-year 

combinations had no school-age children experiencing two or more exposures ≥ 80 ppb 

benchmark, with the other half estimated to have about 1% of all school-age children 

experiencing two or more exposures at or above the 80 ppb benchmark. School-age children 

having four or more 80 ppb benchmark exceedances were limited to only a few study area years 

and, where a non-zero value was estimated, were limited to ≤ 0.5% of the study group. 

5.3.3 Exposure Modeling Results for Simulations of Just Meeting the Existing and 

Alternative 8-hour Ozone Standards 

In this section, we present the exposures estimated when considering the air quality 

adjusted to just meeting the existing O3 NAAQS standard, as well as when considering potential 

alternative 8-hr standard levels (55, 60, 65, 70 ppb) of the existing standard. Comprehensive 

multi-panel displays of exposure results are presented for each of the study groups of interest, 

i.e., all school-age children (5-18), asthmatic school-age children, asthmatic adults (19-95), and 

all older adults (ages 65-95; Figure 5-5 to Figure 5-9, respectively). Included in each display are 

the three exposure benchmarks (60, 70, and 80 ppb), the five years of air quality (2006-2010), for 

the 15 urban study areas. A single multi-panel display is used to present the results for each of 

the four study groups, beginning with the estimated percent of people exposed at least one time 

at or above the selected benchmark levels. Modeled exposures in the 15 study areas and 

considering each benchmark level are presented on the same scale to allow for direct 

comparisons across the multi-panel display. The most notable patterns in the exposure results are 

described here using one study group (i.e., all school-age children), as there is a general 

consistency in the year-to-year variability within each study area across all four study groups. 

Any deviation from the observed pattern will be discussed for the subsequent study group. 

We note that after adjusting to just meet a potential 8-hr ambient standard level of 55 

ppb, there were nearly no people exposed at or above any of the selected benchmark levels, thus 

these data, while modeled, are not presented in detail here. In addition, in one study area 

(Chicago), O3 ambient monitor design values were below that of the existing standard during the 

2008-2010, therefore APEX simulations could not be performed for meeting the existing 

standard for that 3-year period. And finally, we were not able to simulate just meeting an 8-hr 

standard level of 60 ppb or below in the New York study area (see Chapter 4 for details), thus 

APEX simulations for these air quality scenarios could not be performed in New York. 

Figure 5-5 illustrates the exposures estimated for all school-age children in each study 

area with general observations as follows. After adjusting air quality to just meet the existing and 
5-27 

alternative standards, there are virtually no school-age children experiencing a daily maximum 8-

hr exposure ≥ 80 ppb, with very few school-age children exposed at or above the 70 ppb 

benchmark. For example, out of 87 possible study area and year combinations considering air 

quality adjusted to just meet the existing standard (the least stringent standard level considered 

here), only 29 resulted in > 0.1% estimated percent of all school-age children exposed at least 

once at or above the 80 ppb benchmark with the maximum percent of all school-age children 

exposed estimated for St. Louis (1.1%). Ninety-four percent of study area and year combinations 

had fewer than 5% of all school-age children experiencing at least one daily maximum 8-hr 

average exposure at or above 70 ppb considering ambient air quality adjusted to just meeting the 

existing standard, again with a maximum of 8.1% occurring in St. Louis. When considering air 

quality adjusted to just meet an 8-hr ambient standard level of 70 ppb, ≤ 0.2% of all school-age 

children experience at least one daily maximum 8-hr exposure at or above 80 ppb for all study 

area and year combinations, while for 76 or 90 study area and year combinations, ≤ 1% of all 

school-age children exceed the 70 ppb exposure benchmark. This pattern of having very few 

school-age children experiencing daily maximum 8-hr exposures ≥ 70 and 80 ppb is as expected 

given the nature of the air quality adjustment procedure that limits 8-hr ambient concentrations at 

or above the selected potential alternative standard level. 

In contrast, approximately 10-20% percent of all school-age children experience at least 

one daily maximum 8-hr exposure ≥ 60 ppb when considering air quality just meeting the 

existing standard (Figure 5-5). And similar to that mentioned above regarding exposures 

associated with the base air quality, a general year-to-year exposure pattern emerges with respect 

to study area and year. For the Northeastern (Boston, New York), Mid-Atlantic (Philadelphia, 

Washington DC, Cleveland) and Mid-Western (Chicago, Detroit, and St. Louis) study areas, the 

maximum percent of all school-age children exposed generally occurs during year 2007. For the 

Southern (Atlanta, Dallas, Houston) and Western (Denver, Los Angeles, Sacramento) study 

areas, the maximum exposure occurs during year 2006. Deviations from this temporal exposure 

pattern appear mostly as a result of the standard averaging period, with the 2008-2010 period 

producing equal or greater maximum exposures during either 2008, 2010, or both years and most 

prevalent in the Northeastern and Mid-Atlantic study areas (Baltimore, Boston, New York, 

Philadelphia, Washington DC; note also a trend in Atlanta, Denver, St. Louis). 

The exposure patterns observed for the 60 ppb exposure benchmark remain consistent 

when considering air quality adjusted to just meet a 70 ppb ambient standard, though the percent 

of all school-age children exposed is less than that observed when considering the air quality 

adjusted to just meet existing standard. Further, 75 of 90 study area and year combinations are 

estimated to have ≤ 10% of all school-age children experience at least one daily maximum 8-hr 

exposure ≥ 60 ppb, though between 10-20% of all school-age children were estimated to be 
5-28 

exposed for a few study area and year combinations (e.g., Atlanta-2006, Chicago-2007 and -

2010, and Houston-2009). When considering air quality adjusted to just meet a 65 ppb standard 

level, the percent of all school-age children experiencing at least one daily maximum 8-hr 

exposure ≥ 60 ppb diminishes to 5% or less for most study areas and years (i.e., 81 of 90 study 

area year combinations). 

All of what has been described regarding the estimated exposures to school-age children 

(i.e., the year-to-year and benchmark level patterns, and the percent of the study group exposed) 

also applies to the exposures estimated for asthmatic school-age children (Figure 5-6). Different 

however would be the relative number of asthmatic school-age children exposed in each study 

area if compared with all school-age children, as the asthma prevalence rates vary by study area 

(Table 5-2), though on average are about 10% of the population of children.

The percent of asthmatic adults (Figure 5-7) experiencing daily maximum 8-hr average 

exposures above the selected benchmark levels is sharply lower than that estimated for all 

school-age children. For example, only three of a possible 84 study area and year combinations 

(Chicago-2007, Houston-2009, and St. Louis-2007) were estimated have > 0.1% of asthmatic 

adults experience a daily maximum 8-hr average exposure ≥ 80 ppb, and only six of a possible 

84 study area and year combinations were estimated have >1% of asthmatic adults experience an 

daily maximum 8-hr average exposure ≥ 70 ppb, all occurring when considering air quality just 

meeting the existing standard. No study area or year combination has more than 10% of 

asthmatic adults estimated to experience at least one daily maximum 8-hr exposure ≥ 60 ppb 

when considering air quality just meeting the existing standard, with 67 of 84 study area and year 

combinations estimated to have 5% or less asthmatic adults experiencing such exposures. 

When considering air quality adjusted to just meeting an 8-hr standard level of 70 ppb, no 

asthmatic adults experience a daily maximum 8-hr average exposure at or above 80 ppb and ≤

0.6% experience a daily maximum 8-hr average exposure ≥ 70 ppb for any study area or year 

combination. Less than 5% of asthmatic adults could experience a daily maximum 8-hr average 

exposure at or above 60 ppb when considering air quality adjusted to just meet a standard level 

of 70 ppb for 88 or 90 possible study area year combinations, with the maximum percent of adult 

asthmatics exposed outside this range occurring in Denver (6.8%-2008) and St. Louis (5.5%-

2007). 

Older adults are estimated to have the fewest exposures above the two highest benchmark 

levels when considering the adjusted air quality. For example, only two of a possible 84 study 

area and year combinations (St. Louis-2007 and Washington DC-2008) were estimated have > 

0.1% of asthmatic adults experience a daily maximum 8-hr average exposure ≥ 80 ppb, and only 

six of a possible 84 study area and year combinations were estimated have > 1% of asthmatic 

adults experience a daily maximum 8-hr average exposure ≥ 70 ppb, all occurring when 
5-29 

considering air quality just meeting the existing standard (Figure 5-8). Also, exceeding the 60 

ppb exposure benchmark appears to be limited to fewer than 5% of all older adults when 

considering air quality adjusted to just meet the existing standard and a standard level of 70 ppb, 

and occurs in < 2% of all older adults when considering a standard level of 65 ppb. 

An example of multi-day exposure results associated with adjusted air quality is provided 

in Figure 5-9. The percent of all school-age children estimated to experience multi-day exposures 

above benchmark levels during each study area’s O3 season is largely limited to two air quality 

scenarios: the existing standard and air quality adjusted to just meeting an 8-hr standard of 70 

ppb. This is because of the small percent of school-age children experiencing even a single 

exposure above the lowest benchmark level when considering standard levels at or below 65 

ppb. In addition, when experiencing multiple exposures, most school-age children appear to have 

at most two days above benchmark levels per O3 season, even when considering the lowest 

benchmark level of 60 ppb. For example, 81 of 87 possible study area and year combinations 

have < 10% of all school-age children experiencing two or more daily maximum 8-hr average 

exposures ≥ 60 ppb when considering an ambient standard level of 75 ppb, while 83 of 90 

possible study area and year combinations have < 5% of all school-age children experiencing 

two or more exposures ≥ 60 ppb when considering an ambient standard of 70 ppb. Increasing the 

stringency of the standard to 65 ppb yields 81 of 90 possible study area and year combinations 

where < 1% of all school-age children experience two or more exposures ≥ 60 ppb. 

Multi-day exposure to the higher exposure benchmarks (either the 70 or 80 ppb) is a rare 

occurrence, even when considering the air quality adjusted to the existing O3 standard. For 

example, there were no school-age children experiencing two or more daily maximum 8-hr 

average exposures above 80 ppb in all but one study area year combination and, and when 

considering that one study year having a non-zero value (St. Louis-2007), the estimated percent 

of all school-age children at or above the exposure benchmark was only 0.1%. Further, 83 of 87 

possible study area and year combinations have < 1% of all school-age children experiencing 

two or more exposures ≥ 70 ppb, also when considering an ambient standard level of 75 ppb. 

An additional presentation of the estimated exposures is provided in Figure 5-10 and 

Figure 5-11 to broadly summarize the number of people in each study group that could 

experience exposures of concern. As a reminder, Figure 5-5 through Figure 5-9 were designed to 

show the variability in estimated exposures across each of the urban study areas, along with the 

exhibiting variability across the years of air quality and two standard averaging periods. In each 

of these two additional figures, the mean number of people at or above benchmark levels in each 

study area was calculated by first averaging the number of people estimated for the two 2008 

standard averaging periods, then averaging the number of people exposed above benchmark 

levels for the five year period (2006-2010). 
5-30 

Figure 5-10 shows the mean number of people experiencing at least one daily maximum 8-

hr average O3 exposure ≥ 60 ppb per O3 season, while at moderate or greater exertion for each of 

urban the study areas and considering the adjusted air quality scenarios. On average, 

approximately 2.3 million school-age children have at least one daily maximum 8-hr average 

exposure ≥ 60 ppb when considering air quality just meeting the existing standard in the 15 

urban study areas (Figure 5-10, top left panel). That estimated number school-age children 

experiencing exposures of concern is nearly cut in half when considering air quality adjusted to 

just meet an 8-hr average ambient standard of 70 ppb, with approximately 1.2 million 

experiencing, on average, at least one daily maximum 8-hr exposure ≥ 80 ppb per O3 season in 

the 15 urban study areas. The mean number of school-age children experiencing at least one 

daily maximum 8-hr average exposure ≥ 60 ppb is further reduced to just under 400,000 when 

adjusting air quality to just meet an 8-hr average ambient standard of 65 ppb, while 

approximately 70,000, on average, are estimated to be exposed at the same level when 

considering air quality adjusted to just meet a standard of 60 ppb. 

As was shown above regarding the percent of each study group experiencing exposures of 

concern, the reduction in exposures with the increasing stringency of the air quality standard 

scenarios are similar to that of school-age children, although the number of people within each 

of the study groups is less. For example, when considering air quality that just meets the existing 

standard in the 15 urban study areas, nearly 250,000 asthmatic children, on average, are 

estimated to experience at least one daily maximum 8-hr average O3 exposure ≥ 60 ppb per O3

season (Figure 5-10, top right panel) compared with 2.5 million school-age children exposed at 

the same benchmark level. Again, fewer people exposed in one study group compared with that 

of another in this case is a function of the smaller study group (asthmatic school-age children) 

being a fraction of the larger exposed study group (all school-age children) although for other 

study groups (e.g., older adults) fewer people exposed is largely a function of less time spent 

outdoors rather than originating from a smaller overall population size. 

Far fewer people are exposed to the 8-hr benchmark level of 70 ppb when compared with 

the 60 ppb benchmark (Figure 5-11). For example, when considering air quality adjusted to just 

meet an 8-hr average ambient standard of 70 ppb, about 94,000 school-age children on average 

are estimated to experience at least one 8-hour exposure at or above the 70 ppb, while over ten 

times as many would experience at least one 8-hour exposure ≥ 60 ppb per O3 season. Again, 

similar patterns in number of people exposed to the 70 ppb benchmark are present across each of 

the exposure study groups with increasing stringency of the ambient standard level, with on 

average a few thousand to a low as a few hundred estimated to experience exposures of concern 

when adjusting air quality to just meet ambient standard levels of 65 and 60 ppb, respectively. 
5-31 

Figure 5-5. Percent of All School-age Children with at Least One Daily Maximum 8-hr 

Average O3 Exposure at or above 60, 70, and 80 ppb (red, green and blue lines) while at 

Moderate or Greater Exertion, 2006-2010 Air Quality Adjusted to Just Meet 8-hr Average 

O3 Standards of 75, 70, 65, and 60 ppb (panels left to right) in 15 Urban Study Areas. Percent of All School-Age Children with at Least One 8-hr Exposure At or Above Benchmark Level While at Moderate or Greater Exertion, Adjusted Air Quality
5-32 

Figure 5-6. Percent of Asthmatic School-age Children with at Least One Daily Maximum 

8-hr Average O3 Exposure at or above 60, 70, and 80 ppb (red, green and blue lines) while 

at Moderate or Greater Exertion, 2006-2010 Air Quality Adjusted to Just Meet 8-hr 

Average O3 Standards of 75, 70, 65, and 60 ppb (panels left to right),15 Urban Study Areas. Percent of Asthmatic School-Age Children with at Least One 8-hr Exposure At or Above Benchmark Level While at Moderate or Greater Exertion, Adjusted Air Quality
5-33 

Figure 5-7. Percent of Asthmatic Adults with at Least One Daily Maximum 8-hr Average 

O3 Exposure at or above 60, 70, and 80 ppb (red, green and blue lines) while at Moderate 

or Greater Exertion, 2006-2010 Air Quality Adjusted to Just Meet 8-hr Average O3

Standards of 75, 70, 65, and 60 ppb (panels left to right) in 15 Urban Study Areas. Percent of Asthmatic Adults (19-95) with at Least One 8-hr Exposure At or Above Benchmark Level While at Moderate or Greater Exertion, Adjusted Air Quality
5-34 

Figure 5-8. Percent of Older Adults with at Least One Daily Maximum 8-hr Average O3

Exposure at or above 60, 70, and 80 ppb (red, green and blue lines) while at Moderate or 

Greater Exertion, 2006-2010 Air Quality Adjusted to Just Meet 8-hr Average O3 Standards 

of 75, 70, 65, and 60 ppb (panels left to right) in 15 Urban Study Areas. Percent of Older Adults (65-95) with at Least One 8-hr Exposure At or Above Benchmark Level While at Moderate or Greater Exertion, Adjusted Air Quality
5-35 

Figure 5-9. Percent of All School-age Children with ≥ 2, ≥ 4, ≥ 6 (red, green, and blue lines) 

Daily Maximum 8-hr Average O3 Exposures at or above 60 ppb while at Moderate or 

Greater Exertion, 2006-2010 Air Quality (x-axes) Adjusted to Just Meet 8-hr Average O3

Standards of 75, 70, 65, 60 ppb (panels left to right) in 15 Urban Study Areas. Percent of All School-Age Children (5-18) with Multiple 8-hr Exposures at or Above 60 ppb While at Moderate or Greater Exertion, Adjusted Air Quality
5-36 

Figure 5-10. Mean Number of People with at Least One Daily Maximum 8-hr Average Exposure at or abo

Moderate or Greater Exertion, 2006-2010 Air Quality Adjusted to Just Meet 8-hr Standards of 75, 70, 65, 

from right to left), in 15 Urban Study Areas. All School-age children (top left panel), asthmatic school-age 

panel), asthmatic adults (bottom left panel), older adults (bottom right panel). 
5-37 

Figure 5-11. Mean Number of People with at Least One Daily Maximum 8-hr Average Exposure at or abo

Moderate or Greater Exertion, 2006-2010 Air Quality Adjusted to Just Meet 8-hr Standards of 75, 70, 65, 

from right to left), in 15 Urban Study Areas. All School-age children (top left panel), asthmatic school-age 

panel), asthmatic adults (bottom left panel), older adults (bottom right panel).
5-38 

5.4 TARGETED EVALUATION OF EXPOSURE MODEL INPUT AND OUTPUT 

DATA 

This section summarizes the results of several targeted evaluations intended to provide 

additional insights to APEX input data or approaches used to estimate exposures (CHAD data 

attributes and activity pattern evaluations, comparison of CHAD outdoor time data with ATUS, 

comparisons of asthmatic outdoor time expenditure and exertion levels to that of nonasthmatics), exposure results for additional exposure populations of interest (outdoor workers, 

school-age children during summers, impact of averting), and model performance evaluations 

(personal exposure measurements and independent ventilation rate estimates compared with 

APEX estimates). Detailed analysis results are provided in Appendix 5G. 

5.4.1 Analysis of Time-Location-Activity Data 

While CHAD is the most comprehensive and relevant source of time-location-activity 

data available for use in our exposure modeling, there are a few limitations to the survey data 

contained therein, many of which are founded in the individual studies from which activity 

patterns were derived (Graham and McCurdy, 2004). CHAD is a collection of related survey 

data, though individual study attributes can range widely (e.g., survey participant ages, region or 

city of residence, time-of-year data collected). We note that many of the assumptions about use 

of these activity patterns in exposure modeling are strengthened by the manner in which they are 

used by APEX. This is done by focusing on selecting the most important individual attributes 

that contribute to variability in human behavior (e.g., age, sex, day-of-week, ambient 

temperature) and linking these attributes of simulated individuals to the population demographics 

of each census tract (see section 5.2.5) and the study area temperatures (section 5.2.4). Further, 

one key lifestyle attribute is also accounted for in generating longitudinal diary profiles by 

simulating both the intra- and interpersonal variability in time spent outdoors (section 5.2.5; Glen 

et al., 2008). 

A few questions may arise as to the representativeness of the CHAD diaries to the 

simulated population. For example, the year of a particular survey study may differ from our 

simulated exposure population by as much as 30 years (i.e., some activity pattern data were 

generated in the 1980s). In addition, there are other personal attributes (e.g., ethnicity, income 

level, lifestyle factors21), health conditions (e.g., asthma, cardiovascular disease), and situational 

factors (e.g., availability of parks and recreation areas) that are not used in creating the simulated 

 

21 Examples of such factors for adults could include married/unmarried, having infants or young children/no 

children. Lifestyle factors for children could include whether the child is active/non-active or whether or not there 

is time spent outdoors. 
5-39 

individuals that could be influential in estimating exposures. Considering this, a number of 

evaluations were performed to answer questions regarding important personal attributes used in 

generating simulated individuals and the general representativeness of the CHAD time-locationactivity data. First though, we summarize the newly acquired activity pattern data now included 

in CHAD compared with data available and used in the 1st draft O3 HREA. 

5.4.1.1 General evaluation of CHAD study data: historical and recently acquired 

data 

The number of diary days having complete information and used by APEX in the O3

HREA is 41,474 (Table 5-3). This is an increase of about 8,700 diaries currently used by APEX 

compared with what was used by APEX in the 1st Draft O3 HREA. Further, there have been eight 

new study data sets incorporated into CHAD and used in our current exposure assessment since 

the previous O3 NAAQS review conducted in 2007, most of which were from recently conducted 

activity pattern studies (see Appendix 5B, Section 5B-4 for more information regarding these 

studies). The diary data included from these new studies have more than doubled the total 

activity pattern data used for 2007 O3 exposure modeling and has increased the number of 

children’s diaries by about a factor of five. Currently, the majority of diaries (54%) from CHAD 

are taken from surveys conducted in the past decade, while the pre-1990s diaries represent less 

than 15% of the total diaries available by APEX. 

5.4.1.2 Exposure-relevant personal attributes included in CHAD and APEX 

simulated individuals 

The survey participants whose diary data are within CHAD were asked a number of 

questions regarding their personal attributes. The number and type of attributes present for 

diaries in CHAD is driven largely by the original intent of the individual study. In our exposure 

assessment, we have strict requirements to simulate individuals using several personal attributes, 

namely age, sex, temperature (as a surrogate for seasonal variation in activity patterns), and dayof-week. These attributes are considered as important drivers influencing daily activity patterns 

(Graham and McCurdy, 2004) and when diaries do not have these particular attributes for a 

particular day, the diary day will not be used by APEX. We compared the representation of these 

and other attributes in the current CHAD used by APEX with that in the 1st draft O3 HREA and 

found strong similarities in the attribute distributions between both databases, suggesting little 

change in the overall composition of the database regarding these influential attributes. 

While there may be other personal or situational attributes that affect daily time 

expenditure (e.g., socioeconomic status, occupation of an employed person), these attributes are 

typically not included in our assessment to generate simulated individuals simply because the 

response to the attribute is missing for most of the study participants/CHAD diary days. For 
5-40 

example, income level is missing for about two-thirds of the CHAD diaries because either the 

original study did not have an income/occupation related survey question or perhaps the 

participant refused to answer the question if it were posed. If one were to select this personal 

attribute in developing a simulated individual’s activity pattern (among using any other attribute 

having missing responses), the pool of diaries available to simulate individuals may be extremely 

limited, likely leading to repetition of diaries used for individuals or groups of similar individuals 

and artificially reducing both intra- and inter-personal variability in time expenditure, or perhaps 

resulting in model simulation failure altogether. This is why personal attributes are carefully 

selected and prioritized according to both their prevalence in CHAD and whether the attribute 

has a known significant influence on activity patterns. 

5.4.1.3 Evaluation of afternoon time spent outdoors for CHAD survey participants 

There have been questions raised regarding the representativeness of the diaries from 

studies conducted in the 1980s and whether there are any recognizable patterns in time 

expenditure in the CHAD diaries across the time period when data were collected. Because time 

spent outdoors is a significant factor influencing daily maximum 8-hr average O3 exposures, we 

evaluated the current collection of CHAD diaries used by APEX for two metrics and considering 

two dimensions: outdoor participation rate (i.e., the percent of people who spent some time 

outdoors during their survey day) and the mean time spent outdoors for where the people spent at 

least one minute outdoors or at least 2 hours outdoors. Because time spent outdoors is an 

important determinant for highly exposed individuals, we summarize the results here for the 

diaries having at least 2 hours of outdoor time here, while all other results are provided in 

Appendix 5G. CHAD diaries were stratified by five age groups (4-18, 19-34, 35-50, 51-64, 65+) 

and three decades (1980s, 1990s, and 2000s) using the year the particular activity pattern study 

was conducted. We note that CHAD is composed of primarily cross-sectional data (single diary 

days per person), thus the trend evaluated over the three decades is changes (if any) in 

participation rate and the time spent outdoors by the composite study population, not within 

individuals. 

Regardless of decade and duration of time spent outdoors, children tended to have the 

highest outdoor participation rate when compared with the other age groups, while the oldest 

adults (aged 65 or greater) tend to have the lowest participation rate. The CHAD diaries from the 

1980’s studies for children ages 4-18 have the highest outdoor participation rate (50%) compared 

to other decades (35-40%) and all other age groups and decade of collection. When considering 

the pool of diaries available for this age group, these 1980’s studies contribute to approximately 

19% of diaries having two or more hours of time spent outdoors during the afternoon. This 

translates to a small effect on the overall outdoor participation rate for diary pools that would 
5-41 

include these earlier studies (39% participation rate) compared to the participation rate excluding 

these studies (36% participation rate). In general, these outdoor participation rates are similar to 

the finding reported recently by Marino et al. (2012) of 37.5%, though estimated for pre-school 

age children. Thus, when considering participation in outdoor activities and the 

representativeness of the CHAD study data from the 1980s, it is unlikely that use of these oldest 

diaries would strongly influence exposure model estimates. 

There is variability in the amount of outdoor time evaluated over the three decades, with 

diaries from the 2000’s studies exhibiting perhaps the lowest range of mean outdoor time (190-

220 min/day) compared with the 1980’s (210-240 min/day) and 1990’s (212-258 min/day) 

studies, a trend perhaps most notable when considering the children’s diaries (a decrease in time 

spent outdoors of about 30 minutes over the three decades). However, the coefficient of variation 

(COV) for each of the age groups and across all decades for the cross-sectional data was 

consistently about 40%, supporting a general conclusion of no appreciable differences in the 

mean time spent outdoors over the three decades of data collection. Thus, when considering all 

diaries having at least 2 hours of afternoon outdoors time and the representativeness of the 

CHAD study data from the 1980s compared with that of the other CHAD study years, inclusion 

of these earlier diaries is also unlikely to have a strong influence on exposure modeling 

outcomes. 

5.4.1.4 Evaluation of afternoon time spent outdoor for ATUS survey participants 

We evaluated recent year (2002-2011) time expenditure data from the American Time 

Use Survey (ATUS) (US BLS, 2012). As was done with the CHAD data set, the purpose was to 

evaluate trends (if any) in outdoor time over the period of time data were collected. A few 

strengths of the ATUS data are (1) its recent and ongoing data collection efforts, (2) large sample 

size (totaling over 120,000 diary days), (3) national representativeness, and (4) that varying diary 

approaches would not be an influential or confounding factor in evaluating trends over time. 

ATUS does however have a few noteworthy limitations when compared with the CHAD 

data: (1) there are no survey participants under 15 years of age, (2) time spent at home locations 

is neither distinguished as indoors or outdoors, and (3) missing or unknown location data can 

comprise a significant portion of an individual’s day (on average, about 40% (George and 

McCurdy, 2009)). To overcome the limitation afforded by the ambiguous home location, we 

identified particular activity codes most likely to occur outdoors (e.g., participation in a sport) to 

better approximate each ATUS individual’s outdoor time expenditure. Missing time was 

circumvented by our focused analysis: about 85% of missing time information occurs outside of 

the hours of interest here (i.e., before 12:00 PM and after 8:00 PM). Data were stratified by the 
5-42 

same five age groups as was done for the CHAD data, though here the time trends were assessed 

over individual survey years. 

When considering person-days having at least 2 hours of time spent outdoors, there were 

no clear trends over the nine year ATUS study period regarding either the participation rate or 

the mean time spent outdoors for any of the age groups. Consistent with CHAD, the participation 

rate of children was greater than that of the other age groups. The range in ATUS diary outdoor 

participation rate (10-20%) for all age groups is lower than that observed for the CHAD data 

(generally between 20-40%), while the range in mean time spent outdoors (190-240 minutes per 

day) was similar to that of the CHAD data. The lower participation rate for ATUS participants is 

not surprising given the lack of distinction regarding time indoors and outdoors while at home 

for ATUS participants and possibly influenced in part by not having any activity patterns for 

children under 15 years old. Overall, results of the ATUS data analysis generally support the 

representativeness of the CHAD data, and while participation in outdoor activities calculated 

using ATUS diaries was less than CHAD diaries, ATUS survey methods obfuscate the strength 

of this finding. 

5.4.1.5 Evaluation of outdoor time and exertion level for asthmatics and nonasthmatics in CHAD 

Due to limited number of CHAD diaries with survey requested health information, all 

CHAD diaries are assumed appropriate for any APEX simulated individual (i.e., whether 

asthmatic, non-asthmatic, or no compromising health condition was indicated), provided they 

concur with age, sex, temperature, and day-of-week selection criteria. In general, the assumption 

of modeling asthmatics similarly to healthy individuals (i.e., using the same time-locationactivity profiles) is supported by the activity analyses reported by van Gent et al. (2007) and 

Santuz et al. (1997), though other researchers, for example, Ford et al., (2003), have shown 

significantly lower leisure time activity levels in asthmatics when compared with individuals 

who have never had asthma. To provide additional support to the assumption that any CHAD 

diary day can be used to represent the asthmatic population regardless of the study participants’ 

characterization of having asthma or not, we first compared participation in afternoon outdoor 

activities at elevated exertion levels among asthmatic, non-asthmatic, and unknown health status 

using the CHAD diaries. We then compared compatible CHAD diary days with literature 

reported outdoor time participation at varying activity levels. 

In the first comparison, participation in afternoon outdoor activities for non-asthmatic 

children and adults in CHAD were found similar when compared with their respective asthmatic 

cohorts (both about 40-50%). Outdoor participation rate for people having unknown asthma 

status, a smaller fraction of the total diaries, varied ±10% from that having known asthma status 

(children were higher, adults were lower). The amount of time spent outdoors by the people that 
5-43 

did so varied little across the two study groups and three asthma categories. On average, CHAD 

diaries from children indicate approximately 21⁄4 hours of afternoon time is spent outdoors, 80% 

of which is at a moderate or greater exertion level, again regardless of their asthma status, known 

or unknown. Slightly less afternoon time is spent outdoors by adults when compared with 

children, and while their participation in moderate or greater exertion level activities is much less 

(about 63%), there was little difference between asthmatic adults and non-asthmatic adults 

considering outdoor time or percent at moderate or greater exertion. 

For the second comparison, the percentage of waking hours outdoors at varying activity 

levels for asthmatics reported in three independent asthma activity pattern studies (Shamoo et al., 

1994; EPRI, 1988; EPRI 1992) were compared to CHAD diary days having similar personal 

attributes and stratified by asthma status. The range in the percent of waking hours outside at 

moderate activity level for CHAD diaries was similar to that estimated using the three 

independent literature sources (2-10%), however the range in percent of outdoor time associated 

with strenuous activities using the CHAD asthmatic diaries extends beyond that of asthmatic 

individuals from the three independent studies by about a factor of two higher. At this time, the 

definitive reason for this difference is unknown though there are a number of potential 

contributing factors. These would include the diary/survey collection methods, how activities 

and their associated activity levels were classified, variable number of study subjects, and survey 

sample selection methods. Overall, given the above mentioned similarities in outdoor time, 

participation, and activity levels, disregarding the survey record asthma status of any CHAD 

diary to simulate asthmatic and non-asthmatic individuals in this exposure assessment is 

reasonably justified based on the available data analyzed. 

5.4.1.6 Evaluation of time spent outdoors by CHAD subjects in four U.S Census 

regions 

Finally, we performed an additional analysis of outdoor time that evaluates the potential 

differences that might exist in CHAD participant activity patterns across geographic regions of 

the U.S. It is possible that broad cultural, climatological and other attributes that vary across the 

U.S. could influence activity patterns, including time spent outdoors. If such differences in time 

spent outdoors were consistent and substantial, assuming the use of activity patterns without 

regard to the CHAD participant’s original geographic region could lead to bias in urban study 

area exposure estimates. The study group of primary interest is school-age children and considers 

important influential variables used in selection of diaries to perform exposure simulations such 

as temperature and day-of-week. Again, being mindful of potential sample size issues associated 

with additional stratification of the CHAD data set, we characterized the U.S into four regions 
5-44 

(Northeast, South, Midwest, and West) based on the U.S. Census.22 When considering these four 

regions alone and the full CHAD data set used (i.e., 41,474 diaries), the number of available 

CHAD diaries is large Table 5-6), though note that nearly 3,000 diaries do not have an identified 

geographic location and would not be used in an exposure simulation that considered geographic 

location. 

Table 5-6. Number and Percent of All CHAD Diaries Used by APEX and Stratified by 

Four U.S. Regions. 

Region 

Number Of CHAD 

Diaries 

Percent of 

Total Diaries 

Midwest (MW) 5257 12.7 

Northeast (NE) 4323 10.4 

South (SO) 14951 36 

West (WE) 13998 33.8 

Missing (XX) 2945 7.1 

When considering the important influential attributes used in developing our diary pools 

(i.e., age group, sex, temperature, and day of week) in addition to region, the number of diaries 

available for simulating individuals is reasonable for most pools, though for some diary pools 

there only a few available diaries (Table 5-7; e.g., school-age children in the Midwest and 

Northeast, either sex, weekend days, with daily maximum temperature ≥ 84 ◦F). Again, that 

criteria alone (i.e., the number of diaries available) is the justification for not using region as a 

diary pool attribute in developing individual activity pattern profiles for the simulated study 

groups because, for some of our study areas, APEX would simply not simulate exposures due to 

lack of sufficient diaries (e.g., Boston, New York, Detroit). However, it may be of some value to 

evaluate whether there are differences in time spent outdoors across these four U.S. regions using 

the available data to better inform discussions regarding how this uncertainty might affect the 

estimated exposures in this HREA. 

As was done in the above activity pattern analyses, we evaluated the distribution of 

afternoon time spent outdoors for school-age children spending at least one minute outdoors and 

for those spending at least two hours of afternoon time outdoors, though also considering region 

as a potential influential factor. Because high O3 concentration days would tend to occur more 

frequently on days when daily maximum temperatures are also high, we chose to focus our 

analysis on the pool comprised of CHAD diaries where daily maximum temperatures were ≥ 84 

◦F. We evaluated both the participation in the event (i.e., the percent of diaries in diary pool with 

afternoon time spent outdoors) and the amount of time per day for those that participated in an 

outdoor event. 

 

22 https://www.census.gov/geo/maps-data/maps/pdfs/reference/us_regdiv.pdf 
5-45 

Table 5-7. Number of CHAD Diaries for All School-age Children, Stratified by Four U.S. 

Regions and Diary Pool Attributes. 

Region Sex Daily Maximum 

Temperature (◦F) 

Day of 

Week 

Number Of CHAD 

Diaries 

MW 

Female 

≥84 WD 102 

WE 29 

< 55 WD 475 

WE 431 

55-83 WD 286 

WE 267 

Male 

≥84 WD 157 

WE 29 

< 55 WD 443 

WE 408 

55-83 WD 297 

WE 251 

NE 

Female 

≥84 WD 245 

WE 14 

< 55 WD 269 

WE 266 

55-83 WD 201 

WE 132 

Male 

≥84 WD 283 

WE 8 

< 55 WD 254 

WE 270 

55-83 WD 230 

WE 157 

SO 

Female 

≥84 WD 487 

WE 118 

< 55 WD 305 

WE 288 

55-83 WD 824 

WE 783 

Male 

≥84 WD 657 

WE 127 

< 55 WD 347 

WE 322 

55-83 WD 890 

WE 822 

WE 

Female 

≥84 WD 331 

WE 145 

< 55 WD 231 

WE 179 

55-83 WD 976 

WE 726 

Male 

≥84 WD 427 

WE 131 

< 55 WD 354 

WE 252 

55-83 WD 1018 

WE 699 
5-46 

Regarding participation in outdoor activities during afternoon hours, there are general 

consistencies across the four regions (Table 5-8). For example, during weekdays with daily 

maximum temperatures ≥ 84 ◦F, diaries collected from females indicate that between 64-69% 

spent at least one minute of afternoon time outdoors and between 30-41% spent at least 2 hours. 

Under these same conditions, the results for males were also consistent although slightly higher, 

having from 67-70% and 37-41% of days participating in outdoor events of at least one minute 

and two hours, respectively. Diaries for where region was not determined were not consistent 

with these results and indicated greater participation outdoor events, possibly a function of the 

smaller sample size, the general ages of study participants (mean age 14 versus about a mean of 

8-10 for those having region), or the survey itself (all exclusively from the Cincinnati and 

Washington Studies). When considering weekend days, there is greater variability observed in 

outdoor event participation, though much of it appears to be a function of the limited number of 

diaries for analysis, in particular diaries from school-age children residing in the Northeastern 

U.S. (both sexes) and those for Southern school age females. 

Table 5-8. Number and Percent of CHAD Diaries of School-age Children Reporting Time 

Spent Outdoors on Days When Daily Maximum Temperature ≥ 84 ◦F, Stratified by Four 

U.S. Regions, Sex, and Day Type. 

Day of 

Week Sex Region 

CHAD Diaries with Afternoon Time Spent Outdoors 

At Least One Minute At Least Two Hours 

Number 

of Diaries 

Participation 

(% of Diaries) 

Number of 

Diaries 

Participation 

(% of Diaries) 

Weekday 

Female 

MW 66 65 31 30 

NE 167 68 101 41 

SO 314 64 170 35 

WE 228 69 104 31 

XX 26 93 11 39 

Male 

MW 109 69 61 39 

NE 199 70 117 41 

SO 439 67 263 40 

WE 304 71 157 37 

XX 35 100 22 63 

Weekend 

Female 

MW 17 59 9 31 

NE 9 64 8 57 

SO 61 52 25 21 

WE 105 72 55 38 

XX 28 97 15 52 

Male 

MW 21 72 13 45 

NE 6 75 3 38 

SO 87 69 53 42 

WE 103 79 61 47 

XX 34 97 23 66 
5-47 

The amount of time spent outdoors also indicates general consistency across the four U.S. 

regions, along with notable deviations possibly a function of the small number of diaries 

available for analysis. Based on this analysis, we conclude that there is not a substantial 

difference in time spent outdoors across the four regions (and an appropriate number of diaries) 

that would warrant performing additional simulations using a region specific diary pool to 

estimate exposures in the urban study areas. 

 

Figure 5-12. Distribution of Afternoon Time Spent Outdoors for School-age Children on 

Days When Daily Maximum Temperature was ≥ 84 ◦F, Stratified by Four U.S. Regions. 

Females (left panels), males (right panels), weekday days (top panels), weekend days 

(bottom panels) for where at least one minute of afternoon time was spent outdoors. 

5.4.2 Characterization of Factors Influencing High Ozone Exposures 

We investigated the factors that influence people experiencing the highest daily 

maximum 8-hr average exposures. These exposure results in six selected study areas, Atlanta, 

Boston, Denver, Houston, Philadelphia, and Sacramento, considering base air quality and air 

quality just meeting the existing standard were combined with each simulated individual’s 
5-48 

microenvironmental time expenditure during the afternoon hours (12:00 PM through 8:00 PM), 

times of day commonly when daily peak high O3 concentrations occur. We first evaluated the 

relative contribution seven variables23 had on the total explained variability in daily maximum 8-

hr average exposures. We then evaluated the distribution of identified influential variables for 

simulated individuals with the highest exposures. And finally, we identified the 

microenvironmental locations highly exposed people occupied and the activities performed 

within them, given that within an 8-hr time frame most people would likely visit multiple 

locations and perform different activities. 

When considering only person days having the highest daily maximum 8-hr average O3

exposures at any of the six study areas and either air quality scenario and age groupings, 

collectively the main effects of ambient concentrations and outdoor time combined with their 

interaction similarly contribute to approximately 80% of the total explained variance results, 

suggesting that for highly exposed people, the most important influential factors are time spent 

outdoors corresponding with high daily maximum 8-hr average ambient O3 concentrations. 

The distributions of afternoon outdoor time and ambient concentration for highly exposed 

individuals were evaluated considering base air quality and air quality adjusted to just meeting 

the existing standard. As an example, exposure results in Boston indicated that for about half of 

the days, simulated school-age children experiencing high exposures spend about 240 minutes 

outdoors during the afternoon hours along with experiencing daily maximum 8-hr average 

ambient O3 concentrations ≥ 75 ppb. In contrast when adjusting ambient concentrations to just 

meeting the existing standard, for about half of the days, simulated school-age children 

experiencing similar high exposures need to spend about 280 minutes outdoors during the 

afternoon hours along with experiencing daily maximum 8-hr average ambient O3 concentrations 

≥ 60 ppb. Simply put, under conditions of lower ambient concentrations, people need to spend a 

significantly greater amount of time outdoors to experience similar exposures observed at higher 

ambient concentration conditions. 

When considering these highly exposed children, on average about half of children’s total 

afternoon time is spent outdoors on high exposure days, 40% is spent indoors, while only 10% of 

time is spent near-roads or inside motor vehicles. In general, greater than half of the time highly 

exposed children spent outdoors specifically involves performing a moderate or greater exertion 

level activity, such as a sporting activity. While apportionment of afternoon microenvironmental 

time was similar for highly exposed adults in other age groups considered (e.g., 19-35), 

 

23 The seven variables include the main effects of (1) daily maximum 8-hr average ambient O3 concentration, (2-4) 

afternoon time spent outdoors, near-roads, and inside vehicles, and (5) physical activity index (PAI), while also 

including interaction effects from (6) afternoon time outdoors by daily maximum 8-hr average ambient O3

concentration and (7) PAI by afternoon time outdoors. 
5-49 

important high exertion activities performed outdoors also included those associated with paid 

work and performing chores. 

5.4.3 Exposure Results for Additional At-Risk Populations and Lifestages, Exposure 

Scenarios, and Alternative Air Quality Input Data 

5.4.3.1 Exposures estimated for all school-age children during summer months, 

neither attending school nor performing paid work 

As mentioned earlier in describing the longitudinal approach used in the main body of the 

exposure assessment, the sequence of activity diaries for all simulated individuals is determined 

by a user-selected profile variable of interest. In this assessment our longitudinal diary approach 

uses time spent outdoors to link together CHAD diary days, an attempt to appropriately balance 

intra- and inter-personal variability in that variable. For the primary exposure results, all 

available diaries were used in developing any one sample pool without restriction outside of the 

particular characteristics on interest in developing the pool (i.e., age, sex, day-of-week, 

temperature, time spent outdoors). In this targeted simulation in Detroit during three summer 

months of 2007 (June, July, and August), we restricted the diary pool of all school-age children 

to include only those diary days that did not have any time spent inside a school nor had time 

spent performing paid work during any day of the week. The results of this targeted simulation 

were compared to an identical simulation, only differing in that all CHAD diary days were used 

i.e., including any diary day for individuals having school time or paid work, and as was done for 

the main body of this exposure assessment. 

Figure 5-13 indicates that when restricting the CHAD diary pool to include only those 

diaries having no time spent at school or performing paid work activities, there is about 1/3 or 

33% increase in the number (or percent) of all school-age children at or above the 60 ppb 

benchmark, a relationship also consistent across the alternative standards and when considering 

multiple exposures. A similar relationship was found for the other benchmarks (not shown, see 

Appendix 5G). Clearly, based on the analysis results reported in section 5.4.2 regarding factors 

influencing those highly exposed, using only activity pattern data that do not include school or 

work-related events (which would likely occur more so indoors than outdoors) and sampling 

from a pool of diaries consistent with summer temperatures would increase the likelihood 

simulated individuals spend time outdoors and be exposed to concentrations at or above the 

selected benchmarks. This suggests that, for urban study areas having a traditional school 

calendar (i.e., school not in session during the months of June, July and August), exposures at or 

above selected benchmark levels could be underestimated by about 33%. 
5-50 

Figure 5-13. Comparison of the Percent of All School-age Children in Detroit Having Daily 

Maximum 8-hr Average O3 Exposures at or above 60 ppb while at Moderate or Greater 

Exertion, June-August 2007. Using all available CHAD diaries (“All CHAD Diaries”) or 

using CHAD diaries having no time spent in school or performing paid work (“No 

School/Work Diaries”). 

5.4.3.2 Exposures estimated for outdoor workers during summer months 

A targeted APEX simulation was performed for the Atlanta study area to simulate 

summertime exposures for two hypothetical outdoor worker study groups, people between the 

age 19-35 and 36-55, using 2006 air quality just meeting the existing standard. To do this, both 

the daily and longitudinal activity patterns used by APEX were adjusted to best reflect patterns 

expected for outdoor workers (e.g., a standardized work schedule during weekdays) while also 

maintaining variability in those patterns across various occupation types. Briefly, the distribution 

of all employed individual’s occupations was estimated using data provided by the U.S. Bureau 

of Labor and Statistics (US BLS, 2012b)24 and linked with 144 occupation titles from the 

Occupational Information Network (O*NET)25 identified as having one or more days per week 

where paid work was performed outdoors. These data were then aggregated to twelve broadly 

defined BLS occupation groups, generating a data set containing the number of days per week 

work time would be performed outdoors by that occupation group and properly weighted to 

reflect the population distribution of people employed in each outdoor work group. Then, 

 

24 U.S. employment data by SOC codes were obtained from: http://www.bls.gov/emp/#tables: Table 1.2 

Employment by occupation, 2010 and projected 2020. 25 Additional information is available at http://www.onetonline.org. 
5-51 

existing CHAD diary days reflecting outdoor paid work were identified, isolated and replicated 

to reflect this BLS/O*NET outdoor participation rate and occupation group frequencies. A 

10,000 person simulation was performed by APEX using this adjusted CHAD activity pattern 

database designed to simulate outdoor workers and compared with exposure results generated 

from an identical APEX simulation of all employed people, though differing by using the 

standard CHAD database and population-based modeling approach used in the main body 

HREA. Details regarding the development of CHAD activity patterns used as input to simulate 

outdoor workers, as well as other settings and conditions for APEX is described in Appendix 5G. 

Estimated exposures are presented in Figure 5-14 for one of two age study groups 

investigated (results for both age groups were similar) and considering either a longitudinal 

approach designed specifically to reflect an outdoor worker weekday schedule (top panel) or 

when using our general population-based modeling approach (bottom panel). The results indicate 

that when accounting for a structured schedule that includes repeated occurrences of time spent 

outdoors for a specified study group, all while simulated individuals are likely to be more 

consistently performing work tasks that may be at or above moderate or greater exertion levels, 

there are a greater percent of the study group experiences exposures at or above the selected 

health effect benchmark levels than that estimated using our general population-based modeling 

approach. Outdoor workers are expected to experience more exposures at or above benchmark 

levels, though represent a fraction of the total employed population. It is possible that, in using 

the general population-based approach along with the longitudinal algorithm that accounts for 

within and between variability in outdoor time, a number of outdoor workers are incidentally 

simulated and represent a significant portion of those who experienced exposures at or above 

benchmark levels. 26 However, the differences between exposures estimated for the two 

longitudinal approaches become much greater when considering the percent of people 

experiencing multiple exposure days at or above benchmark levels, primarily when considering 

the 60 ppb benchmark. For example, 2% or less of the general population-based exposure group 

was estimated to have two or more daily maximum 8-hr exposures ≥ 60 ppb, while >17% of 

specifically simulated outdoor workers were estimated to experience exposures at or above that 

exposure benchmark.

 

26 Approximately 30% of our outdoor worker study group were estimated to experience at least one daily maximum 

exposure ≥ 60 ppb while at moderate or greater exertion. Assuming outdoor workers comprise 12% of the 

workforce (Appendix 5G, Table 5G-8), outdoor workers experiencing at least one exposure at or above the 60 ppb 

benchmark could contribute a value of 3.6% to the total exposed population (i.e., one comprised of outdoor and 

non-outdoor workers). For the same air quality scenario and using the general population-based approach, we 

estimated 5-8% of a total employed study group (incidentally comprised of outdoor and non-outdoor workers) 

would experience exposures at or above the same benchmark, suggesting 48-75% of people experiencing 

exposures at or above the 60 ppb benchmark have similar activity pattern characteristics as outdoor workers. 
5-52 

Figure 5-14. Percent of Outdoor Workers Ages 19-35 Experiencing Exposures at or above 

Benchmark Levels while at Moderate or Greater Exertion using an Outdoor Worker 

Scenario-based Approach (top panel) and a General Population-based Approach (bottom 

panel), Air Quality Adjusted to Just Meet the Existing Standard in Atlanta, GA, Jun-Aug, 

2006. 
5-53 

5.4.3.3 Exposures estimated for all school-age children when accounting for 

averting behavior 

A growing area of air pollution research involves evaluating the actions people might 

perform in response to high O3 concentration days (ISA, section 4.1.1). Most commonly termed 

averting behaviors, they can be broadly characterized as personal activities that either reduce 

pollutant emissions or limit personal exposure levels. The latter topic is of particular interest in 

this HREA due to the potential negative impact it could have on O3 concentration-response (CR) functions used to estimate health risk and on time expenditure and activity exertion levels 

recorded in the CHAD diaries used by APEX to estimate O3 exposures. To this end, we have 

performed an additional review of the available literature here beyond that summarized in the 

ISA to include several recent technical reports that collected and/or evaluated averting behavior 

data (Graham, 2012). The purpose was to generate a few reasonable quantitative approximations 

that allow us to better understand how averting behavior might affect time-location-activity 

patterns, and then simulate how such personal adjustments might affect our population exposure 

estimates. 

Based on the elements evaluated in our literature review (i.e., air pollution awareness, 

prevalence and duration of averting response), we conclude that most people are aware of alert 

notification systems (in particular those people having compromised health and reside in an 

urban area). We approximate that 30% of all asthmatics (or 15% of the general population) may 

reduce their outdoor activity level on alert days (e.g., KS DOH, 2006; McDermott et al., 2006; 

Wen et al., 2009; Zivin and Neidell, 2009) and that outdoor time/exertion during afternoon hours 

may be reduced by about 20-40 minutes in response to an air quality alert notification 

(Bresnahan et al., 1997; Mansfield et.al, 2006, Neidell, 2010; Sexton, 2011). We used these 

literature derived estimates to generate an adjusted activity diary pool27 used by APEX to 

simulate a 2-day exposure period (August 1-August 2, 2007) in Detroit to approximate the effect 

this degree of averting may have on exceedances of exposure benchmarks. 

When considering base air quality and our designed target to represent averting 

performed by the general population – 15.3 % of all simulated school-age children spent on 

average 44 minutes less time outdoors – resulting in approximately one percentage point or 

fewer children experienced exposures at or above any of the selected benchmark levels (Figure 

5-15, top panel). When considering base air quality and our designed target to represent an 

averting response by the population of asthmatics – 30.3% of simulated asthmatic school-age 

 

27 Because most activity diaries are limited to a single day and the survey participants were not directly asked if they 

altered their daily activities in response to a high air pollution event, we do not know if any diary day represents 

the activities of an individual who averted. Thus it is entirely possible that the “no averting” simulation includes, 

to an unknown extent, individuals who spent less time outdoors than would have occurred if absolutely no 

individuals averted. 
5-54 

children spent on average 44 minutes less time outdoors – resulting in approximately two 

percentage points or fewer experienced exposures at or above any of the selected benchmark 

levels (Figure 5-15, bottom panel). 

Figure 5-15. Percent of All School-age Children (left panel) and Asthmatic School-age 

Children (right panel) Having at Least One Daily Maximum 8-hr Average O3 Exposure at 

or above Benchmark Levels while at Moderate or Greater Exertion During a 2-day 

Simulation in Detroit, Base Air Quality, August 1-2, 2007. Red bars indicate exposure 

results when considering effect of averting. 
5-55 

5.4.3.4 Comparison of APEX estimated exposures using three different base air 

quality data sets: AQS, VNA, and eVNA 

For this exposure assessment, we elected to use a modeling approach to estimate the 

ambient input concentration field and better account for spatial gradients that may exist (Chapter 

4). To support the selection of Voronoi Neighbor Averaging (VNA), we compared exposure 

results separately generated using ambient monitor (AQS), enhanced Voronoi Neighbor 

Averaging (eVNA; a combined VNA and air quality modeling approach), and VNA as input to 

APEX for three study areas: Atlanta, Detroit, and Philadelphia. All APEX settings were 

generally consistent with the simulations discussed previously, though the air quality data 

differed in that the year selected was 2005 (based on the available CMAQ data) and that a 4 Km 

grid was used to define the spatial area for this evaluation rather than census tracts. Daily 

maximum 8-hr average exposures were estimated for asthmatic school-age children residing in 

the same census tracts comprising each air quality domain and summarized in Figure 5-16. 

Figure 5-16. Comparison of APEX Exposure Results Generated for Three Urban Study 

Areas (Atlanta, Detroit, and Philadelphia) using Three Different 2005 Air Quality Input 

Data Sets: AQS, VNA, and eVNA. 
5-56 

Exposure results for all three air quality input data sets were very comparable, with a few 

notable differences. Using AQS monitor concentration data tended to result in a 1-3% greater 

percent of asthmatic school-age children at or above each of the selected benchmark levels when 

compared with exposures estimated using VNA concentrations. While the VNA concentrations 

are based on the AQS monitor data, the approach generates a concentration gradient with 

distance from areas of known concentration that are typically less than the observed values, thus 

yielding fewer individuals exposed to the highest concentrations. Using the eVNA approach to 

generate ambient concentrations tended to result in 2-5% greater percent of asthmatic school-age 

children at or above each of the selected benchmark levels when compared with exposures 

estimated using either the AQS or VNA approaches. This is because at times, the eVNA 

approach estimated high concentrations in areas where no observations were present, based on 

modeling which captures gradients in O3 that may result from nearby sources (see Chapter 4). 

5.4.3.5 Comparison of APEX estimated exposures using two different adjusted air 

quality data sets: quadratic rollback and HDDM 

We elected to use an air quality modeling based approach rather than the previously used 

statistical approach to adjust air quality to just meet the existing and alternative standard levels 

(Chapter 4). To support the selection of the HDDM approach, we compared exposure results for 

the scenario of just meeting the existing standard, separately generated using air quality inputs 

obtained using the quadratic rollback and HDDM method to adjust air quality for the Atlanta 

study area. All APEX settings were generally consistent with the simulations discussed 

previously, though both the air quality data sets used in this comparison differed from that done 

in the main exposure results above in that only the ambient monitor locations were used to define 

the air districts and assumed a 30 km radius of influence, as was done for the 1st draft O3 HREA. 

Daily maximum 8-hr average exposures were estimated for asthmatic school-age children in 

census tracts within 30 km of each air district and summarized in Figure 5-17. 

The quadratic adjusted air quality resulted in slightly fewer percent of asthmatic schoolage children exposed at or above the highest exposure benchmark (80 ppb) when compared with 

exposures estimated using the HDDM model simulation approach, though a significantly greater 

percent of asthmatic school-age children were exposed to the lowest exposure benchmark (60 

ppb) using the quadratic approach. This is because the quadratic approach generally targets the 

highest concentrations for adjustment, while the HDDM approach accounts for changes across 

the full concentration distribution to a varying degree to meet the adjusted concentration level of 

interest. 
5-57 

Figure 5-17. Comparison of Exposure Results Generated by APEX using Two Different 

Air Quality Adjustment Approaches to Just Meet the Existing Standard in Atlanta: 

Quadratic Rollback (left panel) and HDDM-model Simulation (right panel). 

5.4.4 Limited Performance Evaluations 

5.4.4.1 Personal exposure comparisons 

A new evaluation of APEX was performed using a subset of personal O3 exposure 

measurements obtained from the Detroit Exposure and Aerosol Research Study (DEARS) (Meng 

et. al, 2012). For five consecutive days, personal O3 outdoor concentrations along with daily 

time-location activity diaries were collected from 36 adult study participants in Wayne County 

Michigan during July and August 2006.28 An APEX simulation was performed considering these 

same geographic and temporal features, followed with the sub-setting of APEX output data 

according to important personal attributes of the DEARS study participants (5-day collection 

study periods, age/sex distributions, outdoor time, ambient concentrations, and air exchange 

rate). A comparison sample was generated randomly from the complete simulation, selecting for 

50 APEX simulated individuals. 

 

28 The DEARS was primarily designed to estimate human exposure to particulate matter (Rea et al., 2003). 
5-58 

For both data sets and considering the two output variables separately (outdoor time and 

daily exposure), the median daily values for each study participant were ranked, then plotted 

along with each individual’s corresponding minimum and maximum value using each 

individual’s 5 person-days of data (Figure 5-18). In spite of the distinct matching of influential 

personal attributes, over 50% of APEX simulated individuals had median daily O3 exposure 

concentrations above 10 ppb, while only 3% of DEARS participants’ median values exceeded 10 

ppb. These differences between the APEX-modeled daily exposures and DEARS-measured 

personal exposures could possibly be related to differences in precision and assumptions 

regarding both methods, and are discussed with the following. 

Figure 5-18. Distribution of Estimated Daily Average O3 Exposures (top panels) and Daily 

Total Outdoor Time (bottom panels) for DEARS Study Adult Participants (left panels) and 

APEX Simulated Adults (right panels) in Wayne County, MI, July-August 2006. 

Regarding the DEARS measurement data, personal exposures were estimated using a 

passive sampling device and time-averaged over 24-hours. The estimated detection limits for this 

study using this approach were 3 ppb, though commonly reported detection limits for most 

studies using these devices are generally within 5-10 ppb (O3 ISA, section 4.3.1). As shown in 

Figure 5-18, nearly 80% of the sampled individuals had a median daily personal exposure at or 
5-59 

below the DEARS reported 24-hr detection limit of 3 ppb, approximately 85% of sampled 

individuals had a median daily personal exposure at or below a minimum detection value of 5 

ppb, and 97% of sampled individuals had a median daily personal exposure at or below a 

minimum detection value of 10 ppb. Given the significant removal and decay of ambient O3

within indoor microenvironments (indoor is commonly ~60-90% less than ambient 

concentrations; O3 ISA, section 4.3.2), the large amount of daily time spent indoors by most 

people, particularly adults (O3 ISA, section 4.4.1), and that daily average ambient concentrations 

are usually about 30 ppb (O3 ISA, Table 3-7), the 24-hr passive sampler limits of detection are an 

important consideration in understanding the reported DEARS results and other personal O3

exposure measurement studies where, commonly, a substantial portion of daily samples are 

reported as being below the limit of detection (e.g., Sarnat et al., 2006). 

In general, comparisons of the concentrations measured using passive sampling devices 

with those derived from active sampling methods shows reasonable agreement between the two 

approaches, giving some degree of confidence in concentrations estimated using these passive 

sampling devices (e.g., Liu et al., 1993). However, it is not uncommon for these evaluation 

studies to be conducted over longer time periods (days to weeks) due to a lessened confidence in 

their ability to reasonably measure short-term (< 24-hr time averaged samples) low-level O3

concentrations, particularly at levels observed when estimating personal O3 exposures and O3

concentrations in indoor microenvironments (e.g., Winter et al., 2003; Bytnerowicz et al., 2004). 

Further, a greater measurement bias exists between passive and active sampling at higher O3

concentrations (Winter et al., 2003) and potentially the result of a reduced sampling rate due to 

saturation of the passive device receptors. In addition, relative errors in passive measurement of 

up to 90% have been reported for O3 concentrations between 0-10 ppb (Liu et al., 1993). Thus, it 

is possible that the DEARS passively measured personal O3 exposures are biased low due to the 

inability of the sampler to capture short-term (1-min to <1-hr) low indoor O3 concentrations (i.e., 

< 10 ppb) and imprecisely capturing limited instances of short-term (1-min to <1-hr) 

concentration fluctuations that could realistically occur throughout a single day when adult study 

subjects transitioned (albeit infrequently for many study participants) to a high outdoor/ambient 

O3 concentrations microenvironment (>80 ppb). 

To explore this issue further here, Liu et al. (1993) reported that 12-hr outdoor passive 

measurements were strongly correlated (r=0.95, p<0.01) with 12-hr measurements made at a colocated continuous monitoring site, a site having mean 24-hr ambient O3 concentrations of 37.8 

ppb (min 8.3 ppb, max 64.3 ppb). Twelve-hour personal daytime (8AM-8PM) passive O3

exposure samples measured in 23 children ranged from 0.5 to 78.8 ppb (mean 23.9 ppb), 

concentrations that were also well correlated with 12-hr outdoor (r=0.41, p<0.01) and 12-hr 

indoor (r=0.55, p<0.01) passive measurements. Ratios of the daytime 12-hr personal O3
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concentrations to 12-hr ambient O3 concentrations were on average 0.44 (± 0.29 standard 

deviation). Further, time activity diaries collected in the Liu et al. (1993) study subjects indicated 

that on average, the children spent 30% (± 22%) of their time outdoors, and based on evaluations 

in this REA, are an important influential factor driving the personal concentration levels 

(particularly those having the highest exposures) and likely contributing to the overall strong 

correlations between personal and ambient concentrations. 

For comparison, the DEARS 24-hr ambient concentrations measured using a passive 

sampling device ranged from 17-52 ppb (mean 30.2 ppb), lower but generally comparable to the 

Liu et al. 24-hr values. However, the DEARS 24-hr personal exposures ranged from 1-16 ppb 

(mean 3.4 ppb), much lower than a mean of 17.2 ppb approximated for a 24-hr personal 

exposure in the Liu et al. (1993) study, even when assuming the remaining 12-hrs of day was 

spent entirely indoors (i.e., having a mean indoor nighttime concentration of 10.5 ppb reported 

by Liu et al., 1993). Ratios of the DEARS 24-hr personal O3 concentrations to 24-hr ambient O3

concentrations were on average 0.12 (± 0.09 standard deviation) also lower than the values 

reported by Liu et al. (1993) and below that reported by most exposure measurement studies 

discussed in the O3 ISA (generally ranging from 0.3-0.8, section 4.3.3). In addition, the DEARS 

personal O3 exposure measurements were weakly correlated with ambient concentrations 

(r=0.19, p=0.014) and within the lower range of values reported in the O3 ISA for comparisons 

of personal O3 exposures to indoor residential microenvironmental O3 concentrations. 

Substantially less time spent outdoors on average for DEARS study subjects (mean 6.8% of daily 

time) is likely a major factor contributing to the overall weak relationship in the 24-hr personal 

O3 exposure in relation to the 24-hr ambient O3 concentrations. 

Contrary to these uncertainties and influential factors in the DEARS 24-hr personal O3

exposure measurements, modeling O3 exposure is as precise as is allowed by the APEX input 

data. The time resolution and level of the ambient O3 concentrations used in this HREA (1-hr 

and < 1 ppb) combined with that of the time location activity diaries used to represent simulated 

individuals (minutes) result in O3 exposure concentrations that can be calculated for events 

having a minimum duration of 1-minute and at concentrations less than 1 ppb. Simulated 

individuals having variability in exposure concentration of any magnitude will be precisely and 

immediately modeled, including when the individual transitions from short-term high 

concentration exposure events to low concentration exposure events, for any duration of time. 

Thus, simply when accounting for standard methodological differences in calculating exposures, 

particularly when including those that are at or below the measurement device limits of detection 

(such as indoor O3 concentrations), APEX modeled daily exposures would likely in most 

instances be greater (as is observed in Figure 5-18) than that estimated using a passive personal 

measurement device. 
5-61 

It is also possible that the indoor microenvironmental concentrations estimated by APEX 

are biased high, potentially resulting an upward bias in the 24-hour time averaged 

concentrations. Two variables that influence indoor O3 concentrations are the air exchange rate 

and the indoor decay rate. As shown in Appendix 5G Figure 5G-11, the overall distribution of 

AER values estimated for APEX simulated individuals was actually lower than that estimated for 

DEARS study participants, a factor that would lead to generally lower indoor exposures for the 

APEX simulated individuals compared to exposure estimated for the DEARS subjects, if having 

a similar indoor decay rate. APEX estimated exposures account for the O3 decay expected to 

occur within all indoor microenvironments based on findings of Lee et al. (1999). Unfortunately, 

neither of these variables (indoor O3 concentrations and O3 decay rate) were measured in the 

DEARS study so a direct comparison of these two variables cannot be made between the two 

approaches. 

APEX estimated daily average indoor residential microenvironmental concentrations for 

the simulated individuals were divided by daily average ambient concentrations to generate a 

metric comparable to commonly reported Indoor/Outdoor (I/O) ratios (O3 ISA, section 4.3.2). 

Median I/O values of APEX simulated individuals range from 0.1-0.6, having a central tendency 

of about 0.26, while minimum and maximum values occurring on a single day ranged from about 

0.03-0.74 (Figure 5-19). These central tendency values of I/O estimated using APEX are 

consistent with daily mean I/O ratios reported in the O3 ISA for most studies (0.1-0.4), with 

summertime I/O ratios reported as high as 0.58. Higher I/O values are likely related to instances 

where infiltration of outdoor ambient concentrations is increased, such as when windows are 

opened. It is possible that some of the highest I/O ratios estimated here are a result of the highest 

AER used in estimating indoor residential O3 concentrations (Appendix 5G, Figure 5G-11) but 

again, the rate of O3 decay could also play a role if underestimated for the simulated study group. 

In addition, there are limited instances of high AER rates (e.g., AER > 2 hr-1) used for all APEX 

simulated individuals, while high AER for tended to occur for only about half of the DEARS 

study subjects, indicating that there may be instances where APEX indoor simulated 

concentrations are greater than would be expected where an actual residential AER would be less 

variable than that modeled. Thus, it is possible that indoor O3 concentrations could be biased 

high on occasion due to a wider range of variability in AER equally applied across simulated 

individuals’ than should be as well as the potential for underestimation of indoor O3 decay. 
5-62 

Figure 5-19. Distribution of Indoor/Outdoor Concentration Ratios for APEX Simulated 

Adults in Wayne County, MI, July-August 2006. 

This observed difference between the DEARS personal exposure measurements and the 

APEX modeled exposures is important, though given the above discussion and understanding the 

most important influential factors leading to exposures at or above the benchmarks (i.e., 

substantial time spent outdoors and outdoor ambient concentrations) this difference may be of 

limited relevance to the key analysis results in this REA. In this particular evaluation, none of the 

APEX simulated individuals experienced a daily maximum 8-hr exposure at or above any 

exposure benchmark while at moderate or greater exertion. There were however a number of 

person-days where simulated adults had an 8-hr exposure at or above 60 ppb, just not occurring 

at elevated activity levels. In using the existing output data and variables available from the 

simulation, we evaluated these occurrences of elevated daily maximum 8-hr exposures along 

with the total time spent outdoors (Figure 5-20). While the daily maximum 8-hr exposure is 

calculated as a running average and is comprised of all microenvironmental exposures that occur 

for the simulated individual (including those occurring indoors), most critical to the occurrence 

of benchmark exceedances here is when individuals spend a significant amount of their time 

spent outdoors, generally ranging from between 420 to 800 minutes of total outdoor time per 

day. 
5-63 

Figure 5-20. Daily Maximum 8-hr Exposures at or above 60 ppb Estimated by APEX for 

Simulated Adults in Wayne County, MI, July-August 2006. 

A second model-to-measured comparison is provided here that is also relevant to the 

current REA. APEX modeled exposures have previously been compared with personal exposure 

measurements for O3 for the 2007 NAAQS review (US EPA, 2007b). Briefly, APEX O3

simulation results were compared with 6-day personal O3 concentration measurements for 

children ages 7-12 (Xue et al., 2004; Geyh et al., 2000). Two separate areas of San Bernardino 

County were surveyed: urban Upland CA, and the combined small mountain towns of Lake 

Arrowhead, Crestline, and Running Springs, CA. Available ambient monitoring data for these 

locations during the same study years (1995-1996) were used as the air quality input to APEX. 

APEX predicted personal exposures, averaged similarly across a 6-day period, matched 

reasonably well for much of the concentration distribution considering both locations, but tended 

to underestimate exposures at the upper percentiles of the distribution. The average difference 

between the 6-day means was less than 1 ppb, with a range of -11 ppb to +8 ppb, though 

predicted upper bounds for a few averaged exposures having higher exposure concentrations 

were under-predicted by up to 24 ppb (e.g., Figure 5-21). In addition, modeled exposure 

concentration variability was less than that observed in the personal exposure measurements. At 
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the time of analysis, these differences were proposed to be largely driven by under-estimation of 

the spatial variability of the outdoor concentrations used by APEX (US EPA, 2007b). 

Figure 5-21. Means (and range) of 6-day Average Personal O3 Exposures, Measured and 

Modeled (APEX), Upland Ca. Obtained from Figure 8-22 of US EPA (2007b). 

5.4.4.2 Ventilation rate comparisons 

The algorithm used by APEX to estimate minute-by-minute ventilation rate serves as the 

basis for recent updates to the ventilation rate distributions provided in EPAs Exposure Factors 

Handbook (U.S. EPA, 2009b; US EPA, 2011). During the development of the ventilation 

distributions for EPA at that time, two peer-reviewed studies were identified as providing 

somewhat relevant measurement data to evaluate the APEX energy expenditure and ventilation 

algorithm (see Graham, 2009 for additional comparison details). The results of this evaluation 

are summarized below. 

Briefly, Brochu et al. (2006a,b) presents data for ventilation rates derived from tracking 

doubly-labeled water (DLW) consumption/elimination to estimate energy expenditure in healthy 

normal-weight males and females, ages from 1 month to 96 years (n=1,252). Estimates of energy 

expended were combined with a fixed oxygen uptake factor (H=0.21) and using a fixed 

ventilatory equivalent (VQ)29 of 27. The DLW measurement period ranged from 7-21 days, 

resulting in time-averaged metrics that may in some instances provide reasonable estimates for a 

mean daily ventilation rate, but not useful for estimating variability in an individual’s ventilation 

rate over shorter time periods (as is needed by APEX). Further, while DLW is considered by 

some as a ‘gold standard’ for measuring energy expenditure, this characterization would not 

necessarily be directly transferable to approximations that use this measured value (i.e., 

ventilation rate in Brochu et al. (2006a,b) is a calculated value, not measured). Reported 

 

29 The ventilatory equivalent (VQ) is the ventilation rate (VE) divided by the oxygen consumption rate (VO2) 

0

20

40

60

80

1

Concentration (ppb)

Measured APEX range

measured APEX
5-65 

ventilation rates are daily averages for several age groupings (e.g. ages 1 to < 2, 2 to < 5, 5 to < 

7, etc.) along with derived percentiles, each assuming the existence of normally distributed data. 

A 14-day APEX simulation was performed (i.e., the median of 7-21 days for the DLW 

measurement study) to estimate daily ventilation rates for comparison with the time-averaged 

Brochu et al. (2006a) data. Twenty-five thousand people were simulated by APEX to generate 

reasonable numbers of people within each year of age and other potential categorical variables 

(e.g., 100-200, although a few older age groups resulted in having fewer individuals). It is 

important when comparing the two types of data for them to be similar as possible, particularly 

since age and body mass are important influential variables in both estimation methods. A total 

of 9,613 normal-weight individuals were simulated by APEX and used for the following 

analysis. Multi-day ventilation rates were averaged across the 14-day simulation period, yielding 

a mean daily ventilation rate for each person to best represent the DLW time averaging done by 

Brochu et al. (2006a). 

Figure 5-22 compares the APEX simulated individuals body mass normalized mean daily 

ventilation rates with those reported by Brochu et al. (2006a; Table 2, page 684) for several age 

groupings of normal-weight individuals. The two largest differences appear for children of both 

sexes less than age 10 (i.e., Brochu et. al (2006a) estimates are systematically lower than APEX 

estimates) and for ages 16-33 (i.e., APEX estimates are lower than Brochu et al (2006a). Body 

mass normalized ventilation rates also appear to be slightly higher using APEX when 

considering people above age 64 and for both sexes. 

One principal issue identified by us as potentially responsible for some of the above 

differences in ventilation estimates is in the VQ used by Brochu et al. (2006a). A single value of 

27 was used in estimating ventilation rates for both children and adults, however it is widely 

recognized that while a VQ of 27 may be a reasonable approximation for estimating mean 

ventilation rates of adults, it is not appropriate for use in estimating mean ventilation rates in 

children. With this in mind, the Brochu et al. (2006a) ventilation estimates were modified here 

using the VQ estimates offered by Arcus-Arth and Blaisdell (2007). Figure 5-23 illustrates the 

comparison of APEX body mass normalized mean daily ventilation rates with that of Brochu et 

al. (2006a) corrected ventilation estimates. The body mass normalized ventilation estimates for 

school-age children are more similar to those generated by APEX when correcting the Brochu et 

al. (2006a) VQ parameter. Thus, mean ventilation rates generated by APEX are reasonably 

correlated with independent measures from the Brochu et al. (2006a, b) estimates, particularly 

when correcting the Brochu et al. (2006a) ventilation estimates for children using a more 

appropriate estimate of VQ for children. 

In a second study identified for comparison with APEX estimates, Arcus-Arth and 

Blaisdell (2007) provide ventilation estimates for children <19 years of age using energy intake 
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(EI, or calories consumed) and body mass data provided by the USDA’s Continuing Survey of 

Food Intake for Individuals (CSFII; USDA, 2000). Two-day daily average EIs were combined 

with a values of H (i.e., 0.22 for infants, 0.21 for non-infant children) and VQ (i.e., 33.5 for 

children 0-8, 30.6 for boys 9-18, 31.5 for girls 9-18 years old). Again, time-averaging of the data 

may provide reasonable estimates of a daily mean, but offer no variability in ventilation 

estimates for shorter durations. Furthermore, data for both sexes are combined and reported by 

age, with stratified results by sex reported only for aggregated age groups (males and females, 9-

18 years old). 

Figure 5-22. Comparison of Body Mass Normalized Mean Daily Ventilation Rates 

Estimated by APEX (closed symbols) and by Brochu et al., 2006 (open symbols). 

0.0

0.1

0.2

0.3

0.4

0.5

0.6

0.7

0.8

0.9

1.0

1.1

0 10 20 30 40 50 60 70 80 90 100

Body Mass Normalized Mean Daily 

Ventilation (m3/day-kg)

Age (years)

APEX Females

Brochu et al. (2006) Females

APEX Males

Brochu et al. (2006) Males
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Figure 5-23. Comparison of Body Mass Normalized Mean Daily Ventilation Rates in Male 

and Female School-age Children (5-18) when Correcting Brochu et al. (2006a) Results with 

Child Appropriate VQ Estimates. 

A 2-day model simulation was performed by APEX to generate ventilation estimates for 

children to compare with results of Arcus-Arth and Blaisdell (2007).30 APEX ventilation 

estimates were time-averaged to generate mean daily values, and since the data reported in 

Arcus-Arth and Blaisdell (2007) were not separated by sex (outside of broad age categories), the 

APEX estimates were also combined by sex to provide a comparable mean estimate for each 

year of age (5-18). Body mass was also not used as a categorical variable in Arcus-Arth and 

Blaisdell (2007), therefore all APEX simulated individuals were used, regardless of whether they 

could be classified as overweight or of normal weight. In addition, daily ventilation rates for a 

few age groups of children were obtained from Tables 3 and 4 of Brochu et al. (2006a), though 

considering both estimates for normal and overweight individuals (there were no combined data 

available). The Brochu et al. (2006a) results have been corrected for VQ as noted above using 

VQ estimates of Arcus-Arth and Blaisdell (2007) and added for comparison. Figure 5-24 

illustrates ventilation rate estimates from the APEX simulation, along with associated data for 

 

30 Table III, page 103 of Arcus-Arth and Blaisdell (2007) provided body mass normalized ventilation rates. 

0.0

0.1

0.2

0.3

0.4

0.5

0.6

0.7

0.8

0.9

1.0

1.1

4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19

Body Mass Normalized Mean Daily 

Ventilation (m3/day-kg)

Age (years)

APEX Females

Brochu et al. (2006) Females - Corrected VQ

APEX Males

Brochu et al. (2006) Males - Corrected VQ
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school-age children (ages 5-18) obtained from the two publications. Daily mean ventilation 

estimates are quite similar at each year of age, with slightly higher estimates by Arcus-Arth and 

Blaisdell (2007) at ages 9 and above, particularly when compared with APEX ventilation 

estimates. Ventilation estimates are remarkably similar for school-age children for all three 

sources of data, particularly when considering the differences in the type of input data used and 

the varied approaches of APEX, Brochu et al. (2006a), and Arcus-Arth and Blaisdell (2007). 

This overall agreement suggests reasonable confidence can be conferred to the algorithm used by 

APEX to estimate at a minimum, daily mean ventilation rates. 

Figure 5-24. Comparison of Body Mass Normalized Daily Mean Ventilation Rates in 

School-age Children (5-18) Estimated using APEX and Literature Reported Values. 

5.4.4.3 Evaluation of longitudinal profile methodology 

We evaluated the APEX approach used for linking together cross-sectional activity 

pattern diaries to generate longitudinal profiles for our simulated individuals (Appendix 5G, 

Section 5G-3). Of particular interest were how well variability in outdoor participation rate and 

the amount of time expended were represented in our population-based exposure simulations. 

Our goal in developing the most reasonable longitudinal profiles is to capture expected, 

important features of population activity patterns, i.e., there is correlation within an individual’s 

day-to-day activity patterns (though neither exactly repeated nor entirely random for individuals) 

0.0

0.1

0.2

0.3

0.4

0.5

0.6

0.7

0.8

0.9

1.0

1.1

4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19

Body Mass Normalized Ventilation 

(m3/day-kg) 

Age (years)

APEX Mean

Brochu et al. (2006) Normals Mean - Corrected VQ

Arcus-Arth and Blaiedell (2007) Mean

Brochu et al. (2006) OW/OB Mean - Corrected VQ
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and variability across the modeled study group in day-to-day activity patterns (i.e., not every 

simulated individual in the study group does the same activity on the same day). 

The simulated longitudinal profiles indicate the method for linking together crosssectional diaries generates a diverse mixture of people having variable, though expected, activity 

patterns: A small fraction of the simulated population spend a limited amount of afternoon time 

outdoors and occurring at a low frequency across an O3 season, a small fraction consistently 

spends a greater amount (> 2 hours) of time outdoors and occurring at greater frequency (e.g., 

4/5 days per week), while the remaining simulated individuals fall somewhere in between 

regarding participation and total time. While we are not aware of a population database available 

to compare with these simulated results, we are comfortable with the method performance in 

representing the intended variability in longitudinal activity patterns (see section 5G-3 for 

details). 

5.4.4.4 Comparison of exposures estimated using the 2000 and 2010 U.S. Census 

Data 

The population demographics used in to generate the main body exposure results are 

based on the 2000 Census. These include census tract-level counts of urban study area 

population by age and sex, tract-level employment probabilities by age and sex, and tract-to-tract 

commuting patterns. In this HREA, we are modeling the years 2006 to 2010, thus there is some 

uncertainty associated with use of population demographics for a different year than being 

modeled. To assess the extent of this uncertainty, APEX simulations were conducted for seven 

study areas31 using 2010 air quality adjusted to just meet the existing standard and employing the 

2010 Census information and compared estimated exposures with those generated from identical 

APEX runs, though differing by use of the 2000 Census data for input. The exposure study group 

of interest was all school-age children and were evaluated for occurrences of daily maximum 8-

hr exposures above the three exposure benchmarks concomitant with moderate or greater 

exertion. Because the number, identification, and location of tracts can change from one census 

to the next, these new simulations used the county to define the exposure modeling domain. As 

such, results presented here are not necessarily directly comparable to the main body results in 

this chapter. 

Table 5-9 provides the estimated exposure results for each of the seven study areas, 

indicating mostly small differences (<1%) in the percent of school-age children experiencing at 

least one daily maximum 8-hr exposure at or above any of the exposure benchmarks when using 

 

31 The seven study areas modeled here were selected for overall regional representation and to capture areas having 

either negative and positive growth based on a comparison of their respective 2000 and 2010 CSA populations: 

Atlanta (+23.5%), Boston (+3.6%), Cleveland (-2.2%), Detroit (-2.6%), Houston (+25.7%), Los Angeles (9.2%), 

Sacramento (19.0%). http://www.iweblists.com/us/population/CombinedStatisticalAreaPop.html. 
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the 2010 Census data compared to exposures estimated using the 2000 Census data. However, 

for 6 of 7 study areas, the percent of school-age children exposed using the 2000 Census data 

was higher. Sacramento was the only study area where use of the 2010 Census data resulted in 

fewer school-age children experiencing exposures of concern, however, at most the percentage 

point difference was 0.2%. 

Table 5-9. Percent of All School-age Children with Daily Maximum 8-hr Exposures at or 

above Exposure Benchmarks while at Moderate of Greater Exertion, 2010 Air Quality 

Adjusted to Just Meet the Existing Standard, When Using Either 2000 or 2010 Census 

Population Data. 

Exposure 

Benchmark Study Area 

Percent of All School-age Children 

Experiencing at Least One 

Exposure at or above Benchmark 

Exposure 

Difference1

2000 Census 2010 Census Absolute Percent

60 ppb 

Atlanta 13.2 12.1 1.1 8.3 

Boston 11.1 10.8 0.3 2.7 

Cleveland 8.3 7.3 1.0 12.0 

Detroit 15.7 14.9 0.8 5.1 

Houston 14.4 14.3 0.1 0.7 

Los Angeles 6.5 6.4 0.1 1.5 

Sacramento 4.3 4.5 -0.2 -4.7 

70 ppb 

Atlanta 1.7 1.4 0.3 17.6 

Boston 1.6 1.6 0 0 

Cleveland 0.4 0.4 0 0 

Detroit 2.4 2.2 0.2 8.3 

Houston 2.2 2.1 0.1 4.5 

Los Angeles 0.2 0.3 -0.1 -50.0 

Sacramento 0.6 0.6 0 0 

80 ppb 

Atlanta 0.1 0.1 0 0 

Boston 0 0 0 0 

Cleveland 0 0 0 0 

Detroit 0.1 0.1 0 0 

Houston 0.1 0.1 0 0 

Los Angeles 0 0 0 0 

Sacramento 0 0 0 0 1

 Absolute is the percentage point difference between 2000 and 2010 census generated exposures. Percent is the 

absolute difference relative to the 2000 results, scaled by 100. 

5.5 VARIABILITY AND UNCERTAINTY 

An important issue associated with any population exposure or risk assessment is the 

characterization of variability and uncertainty. Variability refers to the inherent heterogeneity in 

a population or variable of interest (e.g., residential air exchange rates). The degree of variability 

cannot be reduced through further research, only better characterized with additional 
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measurement. Uncertainty refers to the lack of knowledge regarding the values of model input 

variables (i.e., parameter uncertainty), the physical systems or relationships used (i.e., use of 

input variables to estimate exposure or risk or model uncertainty), and in specifying the scenario 

that is consistent with purpose of the assessment (i.e., scenario uncertainty). Uncertainty is, 

ideally, reduced to the maximum extent possible through improved measurement of key 

parameters and iterative model refinement. The approaches used to assess variability and to 

characterize uncertainty in this HREA are discussed in the following two sections. Each section 

also contains a concise summary of the identified components contributing to uncertainty and 

how each source may affect the estimated exposures. 

5.5.1 Treatment of Variability 

The purpose for addressing variability in this HREA is to ensure that the estimates of 

exposure and risk reflect the variability of ambient O3 concentrations, population and lifestage 

characteristics, associated O3 exposure and dose, and potential health risk across the study area 

and for the simulated at-risk study groups. In this HREA, there are several algorithms that 

account for variability of input data when generating the number of estimated benchmark 

exceedances or health risk outputs. For example, variability may arise from differences in the 

population residing within census tracts (e.g., age distribution) and the activities that may affect 

population and lifestage exposure to O3 (e.g., time spent inside vehicles, time performing 

moderate or greater exertion level activities outdoors). A complete range of potential exposure 

levels and associated risk estimates can be generated when appropriately addressing variability in 

exposure and risk assessments; note however that the range of values obtained would be within 

the constraints of the input parameters, algorithms, or modeling system used, not necessarily the 

complete range of the true exposure or risk values. 

Where possible, we identified and incorporated the observed variability in input data sets 

to estimate model parameters within the exposure assessment rather than employing standard 

default assumptions and/or using point estimates to describe model inputs. The details regarding 

variability distributions used in data inputs are described in Appendix 5B. To the extent possible 

given the data available for the assessment, we accounted for variability within the exposure 

modeling. APEX has been designed to account for variability in some of the input data, 

including the physiological variables that are important inputs to determining ventilation rates. 

As a result, APEX addresses much of the variability in factors that affect human exposure. 

Important sources of the variability accounted for in this analysis are summarized in Appendix 

5D. 
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5.5.2 Characterization of Uncertainty 

While it may be possible to capture a range of exposure or risk values by accounting for 

variability inherent to influential factors, the true exposure or risk for any given individual within 

a study area is unknown, though can be estimated. To characterize health risks, exposure and risk 

assessors commonly use an iterative process of gathering data, developing models, and 

estimating exposures and risks, given the goals of the assessment, scale of the assessment 

performed, and limitations of the input data available. However, significant uncertainty often 

remains and emphasis is then placed on characterizing the nature of that uncertainty and its 

impact on exposure and risk estimates. 

The HREA’s for the previous O3, NO2, SO2, and CO NAAQS reviews each presented a 

characterization of uncertainty of exposure modeling (Langstaff, 2007; US EPA 2008, 2009a, 

2010). The qualitative approach used in this and other HREAs is described by WHO (2008). 

Briefly, we identified the key aspects of the assessment approach that may contribute to 

uncertainty in the exposure and risk estimates and provided the rationale for their inclusion. 

Then, we characterized the magnitude and direction of the influence on the assessment results 

for each of these identified sources of uncertainty. Consistent with the WHO (2008) guidance, 

staff scaled the overall impact of the uncertainty by considering the degree of uncertainty as 

implied by the relationship between the source of uncertainty and the exposure concentrations. A 

qualitative characterization of low, moderate, and high was assigned to the magnitude of 

influence and knowledge base uncertainty descriptors, using quantitative observations relating to 

understanding the uncertainty, where possible. A summary of the key findings of those prior 

characterizations that are most relevant to the current O3 exposure assessment are provided in 

Table 5-10. 
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Table 5-10. Characterization of Key Uncertainties in Historical and Current Exposure Assessments using 

Sources of Uncertainty 

Historical Uncertainty Characterization 

Influence of 

Uncertainty on 

Exposure/Intake Dose 

Estimates Knowledge- base 

Category Element Direction Magnitude Uncertainty Comments 

Ambient Monitoring Concentrations 

Database Quality Both Low Low 

All ambient pollutant measurements available fAQS are both comprehensive and subject to qucontrol. 

Instrument Measurement Error Over Low Low Mean bias estimated as 1.2% (CV of 4.4%). Se

Table 2 and Figure 6 of Langstaff (2007). 

Missing Data Substitution Method Both Low Low 

Overall completeness of data yield negligible mbias (~0) along with an estimated standard devof 4 ppb when replacing missing values. See T3 of Langstaff (2007). 

Temporal Representation Both Low Low 

Appropriately uses 1-hr time-series of O3

concentrations for 5 years. No missing data for hour input to APEX. 

Spatial Representation: Large Scale Both Low Low Tens of monitors used in each study area. Spatial Representation: Neighborhood Scale (1) Both Low Low 

Spatial interpolation using jackknife method (removal of a single monitor) yielded generally unbiased observed/predicted ratios (mean 1.06having an estimated standard deviation of 0.2. Langstaff (2007). 

Spatial Representation: Neighborhood Scale (2) Over Low Low 

When reducing the APEX radius setting from aunlimited value (actual value used) to 10 km (i.ethe tendency would be to more accurately repreexposure), a smaller fraction (1-3 percentage pof population exceeds benchmark levels. See Figures 7 – 9 of Langstaff (2007). 
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Sources of Uncertainty 

Historical Uncertainty Characterization 

Influence of 

Uncertainty on 

Exposure/Intake Dose 

Estimates Knowledge- base 

Category Element Direction Magnitude Uncertainty Comments 

Spatial Representation: Local Scale VNA estimates 

Both Low Low - Moderate 

Scenario-based evaluation in three study areas indicated small differences in exposure results comparing ambient monitor data or statistically interpolated concentrations to 4 Km grid as an to APEX (Figure 5-16). General dependencies 

approaches used could lead to observed lack odistinction in exposure results. 

Spatial Representation: Vertical Profile Both Moderate Moderate 

Differences between ground-level (0-3 meters) building rooftop sited (25 meters) monitor concentrations can be significant. Most importause of higher elevation monitors would tend to overestimate ground-level exposures (i.e., for wtime is spent outdoors). 

Adjustment of Air Quality to Simulate Just Meeting the Existing Standard 

Quadratic Approach Both Low - Moderate Moderate 

Variable differences (e.g., none to a factor of twthree) in the estimated number of people exposacross study areas when using differing 3-year back periods for a single year of air quality (Langstaff, 2007). 

HDDM Simulation Approach Both Low - Moderate Low - Moderate 

Expected patterns in both air quality and exposresult from HDDM/emissions reduction approac(full distribution affected rather than only upper percentiles, Figure 5-17). Variable differences remain (e.g., none to a factor of two or three) in estimated percent of people exposed across stareas when using differing 3-year roll-back perifor 2008 air quality (Figures 5-5 to 5-9). New Yostudy area could not be simulated to just meet and 55 ppb alternative standards. 
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Sources of Uncertainty 

Historical Uncertainty Characterization 

Influence of 

Uncertainty on 

Exposure/Intake Dose 

Estimates Knowledge- base 

Category Element Direction Magnitude Uncertainty Comments 

APEX: General Input Databases 

Population Demographics and Commuting (US Census) 

Both Low Low 

Comprehensive and subject to quality control. Differences in 2000 data versus modeled years (2006-2010) are likely small when estimating percent of population exposed. Direct comparisexposures estimated using 2000 and 2010 Cendata in seven study areas indicate small differethough 6 of 7 indicated that exposures estimateusing the 2000 Census data were greater than estimated using the 2010 Census data. 

Activity Patterns (CHAD) Both Low - Moderate Low- Moderate 

Comprehensive and subject to quality control. Significantly increased number of diaries used estimate exposure from prior review and 1st draHREA for this review (Table 5-3). Thoroughly evaluated trends and patterns in historical data major issues noted with use of historical data to represent current patterns (Figures 5G-1 and 5Compared outdoor participation and time with Adata base – CHAD participation is higher than ATUS, likely due to ATUS survey methods. Actdata for asthmatics generally similar to nonasthmatics (Tables 5G2-to 5G-5). There is little indication of regional differences in time spent outdoors though sample size may be a limiting in drawing significant conclusions. Remaining uncertainty exists with other influential factors tcannot be accounted for (e.g., SES, region/locaparticipation in outdoor events and associated amount of time). 

Meteorological (NWS) Both Low Low 

Comprehensive and subject to quality control, fmissing values. Limited application in selecting CHAD diaries and AERs. However, while using years of varying meteorological conditions, the 2006-2010 MET data set may not reflect the fusuite of conditions that could exist in future air quality scenarios. 
5-76 

Sources of Uncertainty 

Historical Uncertainty Characterization 

Influence of 

Uncertainty on 

Exposure/Intake Dose 

Estimates Knowledge- base 

Category Element Direction Magnitude Uncertainty Comments 

Poverty Status (US Census) Weighted Asthma Prevalence (CDC) 

Both Low Low- Moderate 

Data used are from a peer-reviewed quality controlled source. Application accounts for variin most important influential variables (age, sexregion, poverty) though possible that variability microscale prevalence not entirely represented

APEX: Microenvironmental Concentrations 

Outdoor Near-Road and Vehicular: Proximity Factors 

Both Low Low- Moderate 

Uncertainty in mean value used approximated apercentage points. See Figure 10 and Table 7 oLangstaff (2007). May be of greater importance certain study areas or under varying conditionsthough even with this mean difference, in-vehicpenetration/decay decreases exposures and heimportance of in-vehicle microenvironments. 

Indoor: Near-Road Over Low Low

Expected reduction in O3 for people residing ne

roads not modeled here, but when included, thea small reduction (~3%) in the number of peoplexperiencing exposure above benchmark levels (Langstaff, 2007). 

Indoor: Air Exchange Rates Both Low Moderate 

Uncertainty due to random sampling variation vbootstrap distribution analysis indicated the AE

and GSD uncertainty for a given study area tenrange to at most from fitted ±1.0 GM and ± 0.5 hr-1. Non-representativeness remains an import

issue as city-to-city variability can be wide rang(GM/GSD pairs can vary by factors of 2-3) and available for city-specific evaluation are limited (Langstaff, 2007). Also, indoor exposures are estimated as not important to daily maximum 8average O3 exposure. 
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Sources of Uncertainty 

Historical Uncertainty Characterization 

Influence of 

Uncertainty on 

Exposure/Intake Dose 

Estimates Knowledge- base 

Category Element Direction Magnitude Uncertainty Comments 

Indoor: A/C Prevalence (AHS) Both Low Low 

Comprehensive and subject to quality control, estimated 95th percentile confidence bounds ra

from a few to just over ten percentage points, thsome urban areas use older year data (Table 9 Langstaff, 2007). Note, variable indicates presence/absence not actual use. Also, indoor exposures are estimated here as limited in importance to daily maximum 8-hr average exposures and sensitivity analyses in NO2 HRE(in-vehicle was most influential exposure ME) concluded indoor prevalence variable was of limimportance. 

Indoor: Removal Rate Both Low Low 

Greatest uncertainty in the input distribution regarded representativeness, though estimated 

unbiased but correct to within 10% (Langstaff, 2007). 

Vehicular: Penetration Factors Both Low Moderate 

Input distribution is from an older measurement study though consistent with recent, albeit limitedata. 
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Sources of Uncertainty 

Historical Uncertainty Characterization 

Influence of 

Uncertainty on 

Exposure/Intake Dose 

Estimates Knowledge- base 

Category Element Direction Magnitude Uncertainty Comments 

APEX: Simulated Activity Profiles 

Longitudinal Profiles Under Low - Moderate Moderate 

Depending on the longitudinal profile method selected, the number of people experiencing multiple exposure events at or above a selected level could differ by about 15 to 50% (see AppeB, Attachment 4 of NO2 REA). Long-term diary 

profiles (i.e., monthly, annual) do not exist for a population, limiting the evaluation. The general population-based modeling approaused for main body HREA results does not assrigid schedules, for example explicitly represen5-day work week for employed people. Howevewhen considering such scheduling (e.g., outdooworkers or all children spending entire summer season not in-school), estimated exposures are greater than when not considering rigid weekly/seasonal schedules. For our hypotheticoutdoor worker scenario, the number of multidaexposures at or above benchmark levels was primarily affected (though mainly the 60 ppb levFigure 5-14), while both percent of children experiencing single and multiday exposures weincreased by about 30% when simulating a rigid schedule (Figure 5-15). 

Commuting Both Low Moderate 

New method used in this assessment is designlink Census commute distances with CHAD vehdrive times. Considered an improvement over tformer approach that did not match distance antime. While vehicle time accounted for through selection, not rigidly scheduled. However, In-veexposures are not important drivers for people exceeding benchmark levels (section 5.4.2). 

At-Risk Population and Lifestages Both Low Low – Moderate An updated evaluation shows activity patterns o

asthmatics are similar to that of non-asthmatics (section 5.4.1, Tables 5G-2 to 5G-5). 
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Sources of Uncertainty 

Historical Uncertainty Characterization 

Influence of 

Uncertainty on 

Exposure/Intake Dose 

Estimates Knowledge- base 

Category Element Direction Magnitude Uncertainty Comments 

APEX: Physiological Processes 

Body Mass (NHANES) Unknown Low Low 

Comprehensive and subject to quality control, though older (1999-2004) than current simulatepopulation, possible small regional variation is represented by national data. 

NVO2max Unknown Low Low Upper bound control for unrealistic activity leve

rarely used by model, thus likely not very influe

RMR Unknown Low Low 

Approach from older literature (Schofield, 1985used in ventilation equation. Note ventilation raestimates are reasonable. 

METS distributions Over Low - Moderate Low - Moderate 

APEX estimated daily mean METs range from 0.1 to 0.2 units (between about 5-10%) higher tindependent literature reported values (Table 1Langstaff, 2007). However, shorter-term values of greater importance in this assessment. 

Ventilation rates Over Low - Moderate Low - Moderate 

APEX estimated daily ventilation rates can be greater (2-3 m3/day) than literature reported 

measurement values (Table 25 of Langstaff, 20though if accounting for measurement bias this minimizes the discrepancy (Graham and McCu2005; see Figure 5-23 and Figure 5-24). Also, a shorter-term comparison (hours rather than daiwhile more informative, cannot be performed dlack of data. 

Exposure Benchmark Level 

EVR characterization of moderate or greater exertion 

Over Moderate Moderate 

Given that the EVR serves as a cut point for selecting individuals performing moderate or grexertion activities and is a lower bound value (~percentile), the simulated number of people achieving this level of exercise could be overestimated. 
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5.6 KEY OBSERVATIONS 

Four additional tables are provided to additionally summarize the exposure results across 

all study areas and years of air quality data. Table 5-11 contains the percent of all school-age 

children experiencing at least one exposure at or above the three exposure benchmark levels, 

while Table 5-12 contains the percent of all school-age children experiencing at least two 

exposures at or above the three exposure benchmark levels, with both tables considering results 

associated with each of the adjusted air quality scenarios. Two descriptive statistics are provided 

in each of these two tables using the exposure results for each urban study area: the mean percent 

of persons exposed in each study area per O3 season, averaged across the 5 years simulated;32

and the maximum percent of persons exposed in each study area for an O3 season, capturing the 

year having the highest ambient concentration where adjusted air quality met a particular 

standard level within the 3-year averaging period.33 Two summary tables are provided to capture 

the mean and maximum number of people experiencing at least one daily maximum 8-hr 

exposure at or above 60 ppb (Table 5-13) and 70 ppb (Table 5-14) per O3 season considering the 

2006-2010 adjusted air quality. The number (mean and maximum) of person-days34 for each of 

the two benchmark levels are also included in these two summary tables. 

And finally, Figure 5-25 illustrates the estimated mean and maximum percent of all 

school-age children exposed for each study area when considering the 60 ppb exposure 

benchmark and adjusted air quality scenarios, and using the data provided in Table 5-11 and 

Table 5-12. 

Presented below are key observations resulting from the O3 exposure analysis: 

 General: The estimated percent of any study group exposed at least one time at or above 

the selected exposure benchmark levels were highest considering the base air quality 

though the percent of people exposed varied by study area, year, and benchmark level 

(Appendix 5F). Very few people within any exposure study group, any study area, and 

any year experienced any benchmark exceedances when considering an alternative 8-hr 

standard level of 55 ppb (all are estimated to be < 0.3%, data not shown). 

 

32 For most urban study areas, the sample size is five years based on years simulated and first averaging the two 

2008 values generated for each of the two standard averaging periods. The number of years used in calculating the 

mean for each study area could vary based on the available air quality (e.g., Chicago does not have 3 years 

simulated for just meeting the existing standard during 2008-2010 period because air quality was below the 

existing standard, thus the total sample size for this study area is 3). 33 In this analysis, the maximum year may not necessarily be the same for each urban study area, though all years 

appropriately fall within the scenario of just meeting the particular standard level in that urban study area. 34 The person-day metric reflects the total number of days per O3 season members of the study group experienced an 

exposure at or above a particular benchmark and when compared with the number of exposed study group 

members can broadly indicate an the overall likelihood of multiple exposure days. 
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 Study Group: The percent of all school-age children exposed at or above the selected 

benchmark levels across all study areas, years, and air quality scenarios were similar to 

exposures for asthmatic school-age children (e.g., Figure 5-5 and Figure 5-6, 

respectively) with both of these study groups having consistently higher percent of 

persons exposed than that estimated for asthmatic adults and all older adults (Figure 5-7 

and Figure 5-8, respectively), generally by about a factor of three or more. The percent of 

all older adults experiencing exposures at or above any benchmark level tended to be 

only a few percentage points or less when compared with corresponding benchmark 

exceedances for asthmatic adults. 

 80 ppb Exposure Benchmark: In general, less than 1% of any study group, including all 

school-age children and any urban study area, was exposed at least once at or above the 

highest exposure benchmark, 80 ppb, when considering the existing standard air quality 

scenario (Table 5-11). When considering an 8-hr standard level of 70 ppb, ≤ 0.2% of any 

study group and any study area was exposed at least once at or above that same 

benchmark. When considering an 8-hr standard level of 65 ppb, no simulated individuals 

experienced a daily maximum 8-hr exposure at or above 80 ppb. 

 70 ppb Exposure Benchmark: Less than 10% of any study group, including all schoolage children and any study area, was exposed at least once at or above an exposure 

benchmark of 70 ppb, when considering the existing standard air quality scenario (Table 

5-11). On average, approximately 360,000 school-age children across all 15 urban study 

areas combined would experience at least one 8-hr exposure at or above 70 ppb (Table 

5-14) for that same scenario. In considering a worst-case year of air quality in each urban 

study area however, the number of school-age children exposed could be as high as 

420,000 totaled across the 15 study areas. When considering an 8-hr standard level of 70 

ppb, ≤ 3.5% of any study group and in any study area was exposed at least once at or 

above the 70 ppb benchmark. For all school-age children, this equates to, on average, just 

less than 100,000 exposed in all 15 urban study areas at least once at or above the 70 ppb 

benchmark, even considering the worst-case air quality year simulated in each of the 15 

study areas (Table 5-14). An 8-hr standard level of 65 ppb is estimated to reduce the 

percent of persons at or above an exposure benchmark of 70 ppb to ≤ 0.5% of any study 

group and in any study area, an air quality scenario leading to at most, approximately 

15,000 school-age children exposed in all 15 urban study areas, even considering the 

worst-case air quality year simulated in each of the 15 study areas (Table 5-14). 

 60 ppb Exposure Benchmark: In general, no more than 26% of any study group in any 

study area was exposed at least once at or above the lowest exposure benchmark, 60 ppb, 

when considering the existing standard air quality scenario (Table 5-11, Figure	5‐25). On 
5-82 

average, approximately 2.3 million school-age children are exposed at least once per O3

season to the 60 ppb benchmark when considering all 15 urban study areas combined and 

air quality adjusted to just meet the existing standard (Table 5-13). In considering a 

worst-case year of air quality in each urban study area however, the number of schoolage children experiencing such exposures could be as high as 4.0 million totaled across 

the 15 study areas. When considering a standard level of 70 ppb, < 20% of any study 

group in any study area was exposed at least once at or above that same benchmark. On 

average about 1.2 million school-age children experience at least one 8-hr exposure to 60 

ppb per O3 season considering air quality adjusted to meet a 70 ppb standard level, 

though during a high ambient concentration year within the standard averaging period, 

the number of school-age children exposed per O3 season to this same benchmark could 

be as high as 1.7 million totaled across the 15 urban study areas (Table 5-13). An 8-hr 

standard level of 65 ppbr is estimated to reduce the percent of persons at or above an 

exposure benchmark of 60 ppb to ≤ 10% of any study group and study area. 

 Multi-day Benchmark Exceedances: When considering air quality adjusted to just meet 

the existing standard, multi-day exposure benchmark exceedances are largely limited to 

two or more exceedances of the 60 ppb exposure benchmark, all occurring for < 15% of 

any study group in any study area (e.g., Table 5-12, Figure 5-9). There were no people 

estimated to experience any multi-day exposures at or above 80 ppb for any study group 

in any study area, while ≤ 2.2% of persons were estimated to experience two or more 

daily maximum 8-hr exposures at or above 70 ppb, each considering any adjusted air 

quality scenario. When the number of people exposed and the number of person-days at 

or above the 70 ppb benchmark are very similar in value, this also reflects that finding of 

limited occurrences of multi-day benchmark level exceedances (Table 5-14). For 

example, we estimated 94,000 school-age children could experience at least one daily 

maximum 8-hr exposure at or above 70 ppb when considering an 8-hr ambient standard 

of 70 ppb, while approximately 99,000 school-age children person-days had an 

exceedance of the 70 ppb exposure benchmark (Table 5-14), indicating that on average 

most simulated individuals experienced only a single day at or above the exposure of 

concern (i.e., the person to person-day ratio is 1.05). 

 Targeted Input Data Evaluations: Frequent occurrence and large amounts of afternoon 

time spent outdoors, along with high ambient O3 concentrations are the most influential 

factors when considering the highest exposed individuals. There is no apparent temporal 

trend in the amount of outdoor time or participation in outdoor events when comparing 

historical CHAD diaries (1980s studies) to recently collected diary data (2000s studies); 

regardless, the majority of CHAD data, in particular those from school-age children, are 
5-83 

from studies conducted since 2000. Use of activity pattern data from non-asthmatic 

individuals to represent asthmatics appears reasonably justified based on an evaluation 

indicating their having similar outdoor time expenditure and attaining similar outdoor 

exertion levels. Afternoon time spent outdoors does not differ when considering the 

CHAD data set stratified by four U.S. Census regions, though the number of diaries 

available for the analysis could be a limiting factor in this lack of an observed difference. 

APEX estimated daily exposures in are somewhat comparable to personal exposure 

measurements; however, both over- and under- estimations occurred to varying degrees 

(Figure 5-18; Figure 5-21). APEX estimated ventilation rates were comparable to 

literature provided estimates, particularly those of school-age children (Figure 5-24). 

 Targeted Exposure Scenarios: When considering a modeling approach that more 

rigidly schedules longitudinal time location activity patterns compared with the standard 

longitudinal approach used by APEX, a greater percent of persons experience at least one 

or more exposures at or above benchmark levels. For example, an APEX model 

simulation using only summer time (no school) CHAD diary days for non-working 

school-age children generated approximately 30% more persons at or above exposure 

benchmark levels compared with exposures estimated using our population-based 

modeling approach (Figure 5-13). When accounting for a fraction of the population to 

avert in response to a bad air quality day, approximately 1-2 percentage point fewer 

persons experienced exposures at or above benchmark levels compared with exposures 

estimated using our population based modeling approach (Figure 5-15).

 
5-84 

Table 5-11. Mean and Maximum Percent of all School-age Children Estimated to 

Experience at Least One Daily Maximum 8-hr Average O3 Exposure at or above Selected 

Health Benchmark Levels while at Moderate or Greater Exertion. 

Study Area 

8-hr 

Standard 

Level 

Percent of All School-Age Children Experiencing At Least 

One Exposure at or above Selected 8-hr Benchmark Level1

60 ppb 70 ppb 80 ppb 

mean max mean max mean max 

Atlanta 

75 14.8 19.3 2.8 4.4 0.3 0.7 

70 7.5 10.8 0.7 1.4 0.1 0.2 

65 2.9 4.8 0.2 0.5 0 0 

60 0.6 1.2 0 0.1 0 0 

Baltimore 

75 12.2 19.0 2.0 4.0 0.2 0.4 

70 7.1 11.8 0.7 1.2 0.1 0.1 

65 3.0 5.4 0.2 0.3 0 0 

60 0.6 1.2 0 0 0 0 

Boston 

75 13.8 21.9 2.8 6.6 0.3 1.0 

70 9.0 15.7 1.2 3.2 0.1 0.2 

65 3.4 6.7 0.2 0.5 0 0 

60 0.7 1.7 0 0 0 0 

Chicago 

75 13.7 24.7 3.2 7.5 0.2 0.7 

70 9.2 16.0 1.0 2.7 0 0.1 

65 4.2 8.1 0.2 0.4 0 0 

60 1.2 2.2 0 0.1 0 0 

Cleveland 

75 10.2 18.0 1.4 3.7 0.1 0.2 

70 4.2 9.3 0.3 0.9 0 0 

65 1.1 3.0 0.1 0.2 0 0 

60 0.1 0.4 0 0 0 0 

Dallas 

75 12.9 22.9 1.9 4.5 0.1 0.3 

70 7.5 16.0 0.6 1.5 0 0.1 

65 3.0 7.6 0.1 0.3 0 0 

60 0.8 1.9 0 0.1 0 0 

Denver 

75 17.0 25.6 1.7 4.1 0.1 0.5 

70 10.2 18.9 0.5 1.7 0 0.1 

65 3.8 9.5 0.1 0.4 0 0 

60 0.2 0.5 0 0 0 0 

Detroit 

75 14.1 19.1 2.4 4.2 0.1 0.2 

70 7.3 10.3 0.5 0.9 0 0 

65 2.9 4.6 0.1 0.2 0 0 

60 0.3 0.7 0 0 0 0 

Houston 

75 11.4 17.8 2.3 5.5 0.3 0.7 

70 6.6 11.9 0.8 2.1 0 0.1 

65 2.7 5.7 0.1 0.4 0 0 

60 0.3 0.7 0 0 0 0 

Los Angeles 

75 9.5 10.2 0.6 1.0 0 0.1 

70 4.4 5.0 0.1 0.2 0 0 

65 1.1 1.5 0 0 0 0 

60 0 0.2 0 0 0 0 

New York 

75 10.9 19.0 1.6 3.7 0.1 0.3 

70 3.3 6.6 0.2 0.5 0 0 

65 0 0.1 0 0 0 0 

60 na na na na na na 

Philadelphia 

75 13.8 20.5 2.1 4.2 0.2 0.4 

70 7.1 11.8 0.6 1.5 0 0.1 

65 2.4 4.6 0.1 0.3 0 0 

60 0.6 1.7 0 0.1 0 0 
5-85 

Study Area 

8-hr 

Standard 

Level 

Percent of All School-Age Children Experiencing At Least 

One Exposure at or above Selected 8-hr Benchmark Level1

60 ppb 70 ppb 80 ppb 

mean max mean max mean max 

Sacramento 

75 10.3 16.5 1.6 2.7 0.1 0.2 

70 5.8 10.0 0.4 0.9 0 0 

65 2.7 4.7 0.1 0.2 0 0 

60 0.4 0.8 0 0 0 0 

St. Louis 

75 16.3 25.8 3.3 8.1 0.3 1.1 

70 10.2 16.9 1.0 2.7 0.1 0.2 

65 3.9 7.3 0.1 0.4 0 0 

60 0.6 1.5 0 0 0 0 

Washington 

75 13.2 23.4 2.4 6.0 0.2 0.8 

70 6.6 12.5 0.6 1.4 0 0.1 

65 2.3 5.0 0.1 0.2 0 0 

60 0.3 0.6 0 0 0 0 

1

 The mean is the arithmetic average of the estimated percent of all school-age children exposed across 2006-2010 

year air quality; max is the highest estimated percent of all school-age children exposed in a year. 

na – we were unable to simulate just meeting a standard level of 60 ppb in the New York study area. 

Table 5-12. Mean and Maximum Percent of All School-age Children Estimated to 

Experience at Least Two Daily Maximum 8-hr Average O3 Exposures at or above Selected 

Health Benchmark Levels while at Moderate or Greater Exertion. 

Study Area 

8-hr 

Standard 

Level 

Percent of All School-Age Children Experiencing At Least 

Two Exposures at or above Selected 8-hr Benchmark Level1

60 ppb 70 ppb 80 ppb 

mean max mean max mean max 

Atlanta 

75 6.0 8.9 0.4 0.7 0 0 

70 2.1 3.3 0 0.1 0 0 

65 0.4 0.8 0 0 0 0 

60 0 0.1 0 0 0 0 

Baltimore 

75 4.6 8.4 0.2 0.5 0 0 

70 1.8 3.7 0 0.1 0 0 

65 0.4 0.9 0 0 0 0 

60 0 0.1 0 0 0 0 

Boston 

75 4.5 9.7 0.3 1.1 0 0 

70 2.2 5.5 0.1 0.4 0 0 

65 0.4 1.1 0 0 0 0 

60 0 0.1 0 0 0 0 

Chicago 

75 5.3 11.6 0.5 1.3 0 0 

70 2.5 5.7 0.1 0.2 0 0 

65 0.8 1.8 0 0 0 0 

60 0.2 0.3 0 0 0 0 

Cleveland 

75 3.1 7.5 0.1 0.5 0 0 

70 0.9 2.6 0 0 0 0 

65 0.1 0.5 0 0 0 0 

60 0 0 0 0 0 0 

Dallas 

75 4.8 12.2 0.2 0.8 0 0 

70 2.2 7.1 0 0.1 0 0 

65 0.5 2.0 0 0 0 0 

60 0 0.2 0 0 0 0 
5-86 

Study Area 

8-hr 

Standard 

Level 

Percent of All School-Age Children Experiencing At Least 

Two Exposures at or above Selected 8-hr Benchmark Level1

60 ppb 70 ppb 80 ppb 

mean max mean max mean max 

Denver 

75 7.6 14.4 0.2 0.4 0 0 

70 3.5 9.2 0 0.1 0 0 

65 0.7 2.8 0 0 0 0 

60 0 0 0 0 0 0 

Detroit 

75 5.0 8.6 0.3 0.8 0 0 

70 1.9 3.6 0 0.1 0 0 

65 0.4 1.1 0 0 0 0 

60 0 0 0 0 0 0 

Houston 

75 3.8 6.3 0.2 0.6 0 0 

70 1.5 2.9 0 0.1 0 0 

65 0.3 0.7 0 0 0 0 

60 0 0 0 0 0 0 

Los Angeles 

75 4.1 4.5 0.1 0.1 0 0 

70 1.6 1.8 0 0 0 0 

65 0.3 0.3 0 0 0 0 

60 0 0 0 0 0 0 

New York 

75 3.4 8.0 0.1 0.4 0 0 

70 0.5 1.4 0 0 0 0 

65 0 0 0 0 0 0 

60 na na na na na na 

Philadelphia 

75 5.0 8.7 0.2 0.5 0 0 

70 1.7 3.3 0 0.1 0 0 

65 0.3 0.6 0 0 0 0 

60 0 0.1 0 0 0 0 

Sacramento 

75 3.7 7.4 0.2 0.5 0 0 

70 1.5 3.4 0 0.1 0 0 

65 0.4 0.9 0 0 0 0 

60 0 0.1 0 0 0 0 

St. Louis 

75 7.0 13.8 0.6 2.2 0 0.1 

70 3.2 7.0 0.1 0.3 0 0 

65 0.7 2.0 0 0 0 0 

60 0 0.1 0 0 0 0 

Washington 

75 5.5 12.5 0.4 1.4 0 0 

70 2.0 5.0 0 0.1 0 0 

65 0.4 1.2 0 0 0 0 

60 0 0 0 0 0 0 

1

 The mean is the arithmetic average of the estimated percent of all school-age children exposed across 2006-2010 

year air quality; max is the highest estimated percent of all school-age children exposed in a year. 

na – we were unable to simulate just meeting a standard level of 60 ppb in the New York study area. 

 
5-87 

Table 5-13. Mean and Maximum Number of People and Person-days with at Least One 

Daily Maximum 8-hr Average O3 Exposure at or above 60 ppb while at Moderate or 

Greater Exertion for All Exposure Study Groups, All 15 Urban Study Areas Combined. 

Study Group 

(Total Simulated 

Population) 

8-hr 

Standard 

Level 

Number of People or Person-days with at Least One Daily 

Maximum 8-hr Average Exposure at or above 60 ppb 

Mean per O3 Season Maximum per O3 Season 

People Person-days People Person-days 

All School-age 

Children 

(19,049,557) 

75 2,316,000 4,043,000 3,588,000 7,187,000

70 1,176,000 1,707,000 1,988,000 3,178,000

65 392,000 483,000 762,000 986,000

60 70,000 76,000 156,000 171,000

Asthmatic 

School-age 

Children 

(1,992,762) 

75 246,000 432,000 385,000 779,000

70 126,000 184,000 214,000 345,000

65 42,000 52,000 81,000 108,000

60 7,700 8,600 17,000 20,000

Asthmatic Adults 

(4,993,077) 

75 180,000 258,000 295,000 446,000

70 83,000 107,000 145,000 192,000

65 25,000 29,000 47,000 55,000

60 4,100 4,400 9,000 10,000

Older Adults 

(35,174,540) 

75 282,000 414,000 497,000 806,000

70 129,000 163,000 246,000 334,000

65 38,000 43,000 83,000 97,000

60 6,800 7,100 16,000 17,000

Table 5-14. Mean and Maximum Number of People and Person-days with at Least One 

Daily Maximum 8-hr Average O3 Exposure at or above 70 ppb while at Moderate or 

Greater Exertion for All Exposure Study Groups, All 15 Urban Study Areas Combined. 

Study Group 

(Total Simulated 

Population) 

8-hr 

Standard 

Level 

Number of People or Person-days with at Least One Daily 

Maximum 8-hr Average Exposure at or above 70 ppb 

Mean per O3 Season Maximum per O3 Season 

People Person-days People Person-days 

All School-age 

Children 

(19,049,557) 

75 362,000 418,000 792,000 950,000

70 94,000 99,000 236,000 256,000

65 14,000 15,000 41,000 43,000

60 1,400 1,400 4,500 4,500

Asthmatic 

School-age 

Children 

(1,992,762) 

75 40,000 46,000 88,000 108,000

70 10,000 11,000 27,000 29,000

65 1,700 1,700 4,500 4,600

60 200 200 500 500

Asthmatic Adults 

(4,993,077) 

75 22,000 24,000 46,000 51,000

70 5,100 5,300 12,000 13,000

65 700 700 1,900 1,900

60 100 100 200 200

Older Adults 

(35,174,540) 

75 39,000 43,000 96,000 107,000

70 9,700 10,000 26,000 27,000

65 1,400 1,400 3,800 3,900

60 100 100 400 400
5-88 

Figure 5-25. Incremental Decreases in Percent of All School-age Children Experiencing Daily Maximum 8-

or above 60 ppb, with Increasing Stringency in Adjusted 2006-2010 Air Quality Standard Levels. Average pmaximum percent (right panels), at least one exposure (top panels), at least two exposures (bottom panels) p
5-89 

5.7 REFERENCES 

Ainsworth, B.E.; W.L. Haskell; A.S. Leon; D.R. Jacobs Jr.; H.J. Montoye; J.F. Sallis; R.S. 

Paffenbarger Jr. 1993. Compendium of physical activities: classification of energy costs of 

human physical activities. Medicine & Science in Sports Exercise. 25:71-80. 

Arcus-Arth, A. and J. Blaisdell. 2007. Statistical distributions of daily breathing rates for narrow 

age groups of infants and children. Risk Analysis. 27(1):97-110. 

Bresnahan, B.W.; M. Dickie and S. Gerking. 1997. Averting behavior and air pollution. Land 

Economics. 73:340-357. 

Brochu, P.; J.F. Ducre-Robitaille and J. Brodeur. 2006a. Physiological daily inhalation rates for 

free-living individuals aged 1 month to 96 years, using data from doubly labeled water 

measurements: a proposal for air quality criteria, standard calculations and health risk 

assessment. Human and Ecological Risk Assessment. 12:675-701. 

Brochu, P.; J.F. Ducre-Robitaille and J. Brodeur. 2006b. Supplemental material for physiological 

daily inhalation rates for free-living individuals aged 1 month to 96 years, using data from 

doubly labeled water measurements: a proposal for air quality criteria, standard 

calculations and health risk assessment. Human and Ecological Risk Assessment. 12:1-12. 

Bytnerowicz A.; M.J. Arbaugh; M. Fenn; R. Musselman; P. Padgett; T. Procter; and R. Cisneros. 

2004. Improving Model Estimates of Smoke Contributions to Regional Haze Using LowCost Sampler Systems. 

<https://www.firescience.gov/JFSP_advanced_search_results_detail.cfm?jdbid=%23%26*

%3F8%0A>. 

Burmaster, D.E. 1998. LogNormal distributions for skin area as a function of body weight. Risk 

Analysis. 18(1):27-32. 

EPRI. 1988. A Study of Activity Patterns among a Group of Los Angeles Asthmatics. Research 

Project 940-5. Electric Power Research Institute. Prepared by Roth Associates, November 

1988. 

EPRI. 1992. A Survey of Daily Asthmatic Activity Patterns in Cincinnati. TR-101396. Research 

Project 940-05. Electric Power Research Institute. Prepared by Roth Associates. November 

1992. 

Ford, E.S.; G.W. Heath; D.M. Mannino and S.C. Redd. 2003. Leisure-time physical activity 

patterns among U.S. adults with asthma. Chest. 124:432-437. 

George, B.J. and T. McCurdy. 2009. Investigating the American time use survey from an 

exposure modeling perspective. Journal of Exposure Science and Environmental 

Epidemiology. 21:92-105. 

Geyh, A.S.; J. Xue, H. Özkaynak and J.D. Spengler. 2000. The Harvard Southern California 

chronic ozone exposure study: assessing ozone exposure of grade-school-age children in 

two Southern California communities. Environmental Health Perspectives. 108:265-270. 

Glen, G.; L. Smith; K. Isaacs; T. McCurdy and J. Langstaff. 2008. A new method of longitudinal 

diary assembly for human exposure modeling. Journal of Exposure Science and 

Environmental Epidemiology. 18:299-311. 

Graham, S.E. and T. McCurdy. 2004. Developing meaningful cohorts for human exposure 

models. Journal of Exposure Analysis and Environmental Epidemiology. 14:23-43. 
5-90 

Graham, S.E. and T. McCurdy. 2005. Revised Ventilation Rate (VE) Equations for Use in 

Inhalation-oriented Exposure Models. Washington, DC: EPA Office of Air and Radiation. 

(EPA document number EPA/600/X-05/008, Appendix A). 

<http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=202543>. 

Graham, S. 2009. Response to Peer-review Comments on Appendix A, prepared by S. Graham 

(U.S. EPA). Response is Appendix D of US EPA (2009b). Research Triangle Park, NC: 

EPA Office of Air and Radiation. 

<http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=202543>. 

Graham, S. E. 2012. Comprehensive Review of Published Averting Behavior Studies and 

Available Technical Documents. Memo to Bryan Hubbell, Group Leader, Risk and 

Benefits Group, Office of Air Quality Planning and Standards. (EPA Docket # EPA-HQOAR-2008-0699-0085). 

Isaacs, K. and L. Smith. 2005. New Values for Physiological Parameters for the Exposure Model 

Input File Physiology, text memorandum submitted to the U.S. Environmental Protection 

Agency under EPA Contract EP-D-05-065. NERL WA 10. Alion Science and Technology. 

Found in US EPA. (2009). Risk and Exposure Assessment to Support the Review of the SO2

Primary National Ambient Air Quality Standard. (EPA document number EPA-452/R-09-

007, August 2009). 

<http://www.epa.gov/ttn/naaqs/standards/so2/data/200908SO2REAFinalReport.pdf>. 

Isaacs, K.; G. Glen; T. McCurdy and L. Smith. 2008. Modeling energy expenditure and oxygen 

consumption in human exposure models: accounting for fatigue and EPOC. Journal of 

Exposure Science and Environmental Epidemiology. 18:289–298. 

Kansas Department of Health and Environment. 2006. Environmental Factors, Outdoor Air 

Quality, and Activity Level: Results from 2005 Kansas Behavioral Risk Factor Surveillance 

System. Office of Health Promotion, KDOH, available at: 

<http://www.kdheks.gov/brfss/PDF/cste_report_final.pdf>. 

Langstaff, J.E. 2007. Analysis of Uncertainty in Ozone Population Exposure Modeling, OAQPS 

Staff Memorandum to Ozone NAAQS Review, January 31. Washington, DC: Office of Air 

Radiation. (EPA docket number OAR-2005-0172). Available at: 

<http://www.epa.gov/ttn/naaqs/standards/ozone/s_O3_cr_td.html>. 

Lee, K.; J. Vallarino; T. Dumyahn; H. Ozkaynak; and J.D. Spengler. 1999. Ozone decay rates in 

residences. Journal of the Air and Waste Management Association. 49:1238-1244. 

Lioy, P.J. 1990. The analysis of total human exposure for exposure assessment: a multidiscipline science for examining human contact with contaminants. Environmental Science 

and Technology. 24:938-945. 

Liu, S.-J.; P. Koutrakis; H.H. Suh; J.D. Mulik; and R.M. Burton. 1993. Use of personal 

measurements for ozone exposure assessment: a pilot study. Environmental Health 

Perspectives. 101:318-324. 

Mansfield, C.; F.R. Johnson and G. Van Houtven. 2006. The missing piece: averting behavior 

for children’s ozone exposures. Resource Energy Economics. 28:215-228. 

Marino, A.J.; E.N. Fletcher; R.C. Whitaker and S.E. Anderson. 2012. Amount and 

environmental predictors of outdoor playtime at home and school: a cross-sectional 

analysis of a national sample of preschool-aged children attending head start. Health & 

Place. 18:1224-1230. 
5-91 

McCurdy, T. 2000. Conceptual basis for multi-route intake dose modeling using an energy 

expenditure approach. Journal of Exposure Analysis and Environmental Epidemiology. 

10:1-12. 

McCurdy, T.; G. Glen; L. Smith and Y. Lakkadi. 2000. The National Exposure Research 

Laboratory's consolidated human activity database. Journal of Exposure Analysis and 

Environmental Epidemiology. 10:566-578. 

McDermott, M.; R. Srivastava and S. Croskell. 2006. Awareness of and compliance with air 

pollution advisories: a comparison of parents of asthmatics with other parents. Journal of 

Asthma. 43:235-239. 

McDonnell, W.F.; H.R. Kehrl; S. Abdul-Salaam; P.J. Ives; L.J. Folinsbee; R.B. Devlin; J.J. 

O’Neil and D.H. Horstman. 1991. Respiratory response of humans exposed to low levels of 

ozone for 6.6 hours. Archives of Environmental Health. 46(3):145-150. 

Meng, Q.; R. Williams and J.P. Pinto. (2012). Determinants of the associations between ambient 

concentrations and personal exposures to PM2.5, NO2, and O3 during DEARS. Atmospheric 

Environment. 63:109-116. 

Montoye, H.J.; H.C. G. Kemper; W.H.N. Saris and R.A. Washburn. 1996. Measuring Physical 

Activity and Energy Expenditure. Human Kinetics: Champaign, IL. 

National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: 

Advances and Opportunities. Washington, DC: National Academy of Sciences. 

Neidell, M. 2010. Air quality warnings and outdoor activities: evidence from Southern California 

using a regression discontinuity approach design. Journal of Epidemiology Community 

Health. 64:921-926. 

Rea, A; A. Vette; R. Williams; J. Suggs; L. Sheldon; R. Fortmann; and L. Wallace. 2003. 

Exposure to Airborne Particles and Gases and Apportionment to Major Sources in the 

Detroit Area (The Detroit Exposure Aerosol Research Study). Revised Study Plan after 

Peer Review, September 9, 2003. <http://www.epa.gov/dears/images/study-design.pdf>. 

Santuz, P.; E. Baraldi; M. Filippone and F. Zacchello. 1997. Exercise performance in children 

with asthma: is it different from that of healthy controls? European Respiratory Journal. 

10:1254-1260. 

Sarnat, S.E.; B.A. Coull; J. Schwartz; D.R. Gold; and H.H. Suh. 2006. Factors affecting the 

association between ambient concentrations and personal exposures to particles and gases. 

Environmental Health Perspectives. 114(5):649-654. 

Schofield, W.N. 1985. Predicting basal metabolic rate, new standards, and review of previous 

work. Human Nutrition - Clinical Nutrition. 39C(S1):5-41. 

Sexton, A. L. (2011). Responses to Air Quality Alerts: Do Americans Spend Less Time 

Outdoors?. 

<http://www.apec.umn.edu/prod/groups/cfans/@pub/@cfans/@apec/documents/asset/cfans

_asset_365645.pdf>. 

Shamoo, D.A.; W.S. Linn; R.C. Peng; J.C. Solomon; T.L. Webb; J.D. Hackney and H. Hong. 

1994. Time-activity patterns and diurnal variation of respiratory status in a panel of 

asthmatics: implications for short-term air pollution effects." Journal of Exposure Analysis 

and Environmental Epidemiology. 4(2):133-148. 
5-92 

U.S. Bureau of Labor Statistics. 2012. American Time Use Survey User’s Guide. "Understanding 

ATUS 2003 to 2011," August 2012. <http://www.bls.gov/tus/>. 

U.S. Census Bureau. 2007. 2000 Census of Population and Housing. Summary File 3 (SF3) 

Technical Documentation. <http://www.census.gov/prod/cen2000/doc/sf3.pdf>. Individual 

SF3 files '30' (for income/poverty variables pct50) for each state were downloaded from: 

<http://www2.census.gov/census_2000/datasets/Summary_File_3/>. 

U.S. Department of Agriculture. 2000. Continuing Survey of Food Intake by Individuals (CSFII) 

1994-96, 1998. Agricultural Research Service, CD-ROM, available at: 

<http://www.ars.usda.gov/Services/docs.htm?docid=14531>. 

U.S. EPA. 1986. Air Quality Criteria for Ozone and Other Photochemical Oxidants. Research 

Triangle Park, NC: Office of Health and Environmental Assessment, Environmental 

Criteria and Assessment Office. (EPA document number EPA-600/8-84-020aF-eF). 

Available from the National Technical Information Service, Springfield, VA. (NTIS 

publication number PB87-142949). 

U.S. EPA. 1996a. Review of National Ambient Air Quality Standards for Ozone: Assessment of 

Scientific and Technical Information - OAQPS Staff Paper. Research Triangle Park, NC: 

EPA Office of Air Quality Planning and Standards. (EPA document number EPA/452/R96-007). <http://www.epa.gov/ttn/naaqs/standards/ozone/s_O3_pr_sp.html>. 

U.S. EPA. 1996b. Air Quality Criteria for Ozone and Related Photochemical Oxidants. Research 

Triangle Park, NC: EPA Office of Research and Development, National Center for 

Environmental Assessment. (EPA document number EPA/600/P-93/004aF-cF). 

<http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=2831>. 

U.S. EPA. 2002. Consolidated Human Activities Database (CHAD) Users Guide. 

<http://www.epa.gov/chadnet1/>. 

U.S. EPA. 2005. Guidance on Selecting Age Groups for Monitoring and Assessing Childhood 

Exposures to Environmental Contaminants. (EPA document number EPA/630/P-03/003F). 

<http://www.epa.gov/raf/publications/pdfs/AGEGROUPS.PDF>. 

U.S. EPA. 2006. Air Quality Criteria for Ozone and Related Photochemical Oxidants (Final). 

Research Triangle Park, NC: EPA National Center for Environmental Assessment. (EPA 

document number EPA/600/R-05/004aF-cF). 

<http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=149923>. 

U.S. EPA. 2007a. Review of National Ambient Air Quality Standards for Ozone: Policy 

Assessment of Scientific and Technical Information - OAQPS Staff Paper. Research 

Triangle Park, NC: EPA Office of Air Quality Planning and Standards. (EPA document 

number EPA-452/R-07-007). 

<http://www.epa.gov/ttn/naaqs/standards/ozone/data/2007_07_ozone_staff_paper.pdf>. 

U.S. EPA. 2007b. Ozone Population Exposure Analysis for Selected Urban Areas. Research 

Triangle Park, NC: EPA Office of Air Quality Planning and Standards. 

<http://www.epa.gov/ttn/naaqs/standards/ozone/s_O3_cr_td.html>. 

U.S. EPA. 2008. Risk and Exposure Assessment to Support the Review of the NO2 Primary 

National Ambient Air Quality Standard. Washington, DC: EPA Office of Air and 

Radiation. (EPA document number EPA-452/R-08-008a0, November). 

<http://www.epa.gov/ttn/naaqs/standards/nox/data/20081121_NO2_REA_final.pdf>. 
5-93 

U.S. EPA. 2009a. Risk and Exposure Assessment to Support the Review of the SO2 Primary 

National Ambient Air Quality Standard. (EPA document number EPA-452/R-09-007, 

August). 

<http://www.epa.gov/ttn/naaqs/standards/so2/data/200908SO2REAFinalReport.pdf>. 

U.S. EPA. 2009b. Metabolically Derived Human Ventilation Rates: A Revised Approach Based 

Upon Oxygen Consumption Rates. Washington, DC: EPA National Center for 

Environmental Assessment. (EPA document number EPA/600/R-06/129F). 

<http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=202543>. 

U.S. EPA. 2010. Quantitative Risk and Exposure Assessment for Carbon Monoxide – Amended. 

Research Triangle Park, NC: EPA Office of Air Quality Planning and Standards. (EPA 

document number EPA-452/R-10-009, July). 

<http://www.epa.gov/ttn/naaqs/standards/co/data/CO-REA-Amended-July2010.pdf>. 

U.S. EPA. 2011. Exposure Factors Handbook, 2011 edition. Washington, DC: EPA National 

Center for Environmental Assessment. (EPA document number EPA/600/R-09/052F). 

<http://www.epa.gov/ncea/efh/pdfs/efh-complete.pdf>. 

U.S. EPA. 2012a. Total Risk Integrated Methodology (TRIM) - Air Pollutants Exposure Model 

Documentation (TRIM.Expo / APEX, Version 4.4) Volume I: User’s Guide. Research 

Triangle Park, NC: EPA Office of Air Quality Planning and Standards. (EPA document 

number EPA-452/B-12-001a). <http://www.epa.gov/ttn/fera/human_apex.html>. 

U.S. EPA. 2012b. Total Risk Integrated Methodology (TRIM) - Air Pollutants Exposure Model 

Documentation (TRIM.Expo / APEX, Version 4.4) Volume II: Technical Support 

Document. Research Triangle Park, NC: EPA Office of Air Quality Planning and 

Standards. (EPA document number EPA-452/B-12-001b). 

<http://www.epa.gov/ttn/fera/human_apex.html>. 

U.S. EPA. 2013. Integrated Science Assessment of Ozone and Related Photochemical Oxidants. 

Research Triangle Park, NC: EPA National Center for Environmental Assessment. (EPA 

document number EPA 600/R-10/076F). 

<http://cfpub.epa.gov/ncea/isa/recordisplay.cfm?deid=247492#Download>. 

Winter, S.E.; R.A. Bilonick; J.A. Withum; V.B. Conrad; R.M. Statnick; S.T. Ebelt; H.H. Suh; 

and P. Koutrakis. 2003. A Field Evaluation to Compare the Performance of Personal 

Exposure Multi-Pollutant Samplers vs. Federal Method Monitors at a Central Ambient Air 

Monitoring Station in Steubenville, Ohio. Presented at Air Quality IV Conference, 

Arlington, VA September 23, 2003. 

<http://www.alrc.doe.gov/technologies/coalpower/ewr/air_quality_research/am_monitor/sc

amp.html>. 

van Gent, R.; K. van der Ent; L.E.M. van Essen-Zandvliet; M.M. Rovers; J.L.L. Kimpen; G. de 

Meer and P.H.C. Klijn. 2007. No difference in physical activity in (Un)diagnosed asthma 

and healthy controls. Pediatric Pulmonology. 42:1018-1023. 

Wen, X.J.; L. Balluz and A. Mokdad. 2009. Association between media alerts of air quality 

index and change of outdoor activity among adult asthma in six states, BRFSS, 2005. 

Journal of Community Health. 34:40-46. 

Whitfield, R.; W. Biller; M. Jusko and J. Keisler. 1996. A Probabilistic Assessment of Health 

Risks Associated with Short- and Long-Term Exposure to Tropospheric Ozone. Argonne, 

IL: Argonne National Laboratory. 
5-94 

World Health Organization. 2008. Uncertainty and Data Quality in Exposure Assessment. "Part 

1: Guidance Document on Characterizing and Communicating Uncertainty in Exposure 

Assessment." 

<http://www.who.int/ipcs/publications/methods/harmonization/exposure_assessment.pdf. 

Xue, J.; T. McCurdy; J. Spengler and H. Özkaynak. 2004. Understanding variability in time 

spent in selected locations for 7-12 year old children. Journal of Exposure Analysis and 

Environmental Epidemiology. 14(3):222-33. 

Zivin, J.G. and M. Neidell. 2009. Days of haze: environmental information disclosure and 

intertemporal avoidance behavior. Journal of Environmental Economic Management. 

58(2):119-128. 
6-1 

6 CHARACTERIZATION OF HEALTH RISKS BASED ON 

CONTROLLED HUMAN EXPOSURE STUDIES 

6.1 INTRODUCTION 

This chapter presents information regarding the methods and results for a controlled 

human exposure-based ozone (O3) health risk assessment that builds upon the methodology used 

in the assessment conducted as part of the O3 NAAQS review completed in 2008 and also 

introduces a new method for estimating risk. In the previous review, EPA conducted a health risk 

assessment that produced risk estimates for the number and percent of school-aged children, 

asthmatic school-aged children, and the general population experiencing lung function 

decrements associated with O3 exposures for 12 urban study areas, where lung function is 

measured as forced expiratory volume in one second (FEV1). That portion of the risk assessment 

was based on exposure-response (E-R) relationships developed from analysis of data from 

several controlled human exposure studies which were combined with population-level exposure 

distributions developed for children and adults. Risk estimates for lung function decrements were 

developed for recent air quality levels and for just meeting the existing daily maximum 8-hour 

(8-hr) average standard and several alternative 8-hr standards. The methodological approach 

followed in the last risk assessment and risk estimates resulting from that assessment are 

described in the 2007 Staff Paper (U.S. EPA, 2007a). 

The goals of the current O3 risk assessment are to provide estimates of the number and 

percentage of select study groups that would experience adverse respiratory effects associated 

with recent O3 levels and with meeting the existing and potential alternative O3 standards in 

specific urban study areas; and to develop a better understanding of the influence of various 

inputs and assumptions on the risk estimates. The current assessment includes estimates of risks 

of lung function decrements in school-aged children (ages 5 to 18), asthmatic school-aged 

children, and the adult population (19 and above). We recognize that there are many sources of 

uncertainty in the inputs and approach used in this portion of the health risk assessment which 

make the specific estimates uncertain, however, we have sufficient confidence in the magnitude 

and direction of the estimates provided by the assessment for it to serve as a useful input to 

decisions on the adequacy of the O3 standard and risk reductions associated with alternative 

standards. 

We are estimating lung function risk using two methodologies in this review. The 

primary results are based on a new model that estimates FEV1 responses for individuals 

associated with short-term exposures to O3 (McDonnell, Stewart, and Smith, 2007, 2010; 

McDonnell et al., 2012). We refer to this model as the McDonnell-Stewart-Smith (MSS) model. 

We also provide estimates following the methodology used in previous reviews which provides 
6-2 

population level estimates of the percent and number of people at risk. We refer to this model as 

the population E-R model used in previous reviews. Both of these models are implemented in the 

air pollution exposure model APEX (U.S. EPA, 2012a,b). Following this introductory section, 

this chapter discusses the scope of the controlled human exposure study based risk assessment, 

describes the risk models, and provides key results from the assessment. The results of sensitivity 

analyses are reported and key uncertainties are identified and summarized. More detailed 

descriptions of several parts of the analyses are included in appendices that accompany this 

Health Risk and Exposure Assessment (HREA). 

6.1.1 Development of Approach for Current Risk Assessment 

The lung function risk assessment described in this chapter builds upon the methodology 

and lessons learned from the risk assessment work conducted for previous reviews (U.S. EPA, 

1996, 2007a). The current risk assessment also is based on the information evaluated in the ISA 

(U.S. EPA, 2013). The general approach used in the current risk assessment was described in the 

Scope and Methods Plan for Health Risk and Exposure (U.S. EPA, 2011), that was released to 

the CASAC and general public in April 2011 for review and comment and which was the subject 

of a consultation with the CASAC O3 Panel in May 2011. The first and second drafts of this 

HREA were reviewed by CASAC in September 2012 and March 2014. The approach used in the 

current risk assessment reflects consideration of the comments offered by CASAC members and 

the public on the Scope and Methods Plan and the two draft HREAs. 

Controlled human exposure studies involve volunteers, primarily healthy adults, who are 

exposed while engaged in different exercise regimens to specified levels of O3 under controlled 

conditions for specified amounts of time. For the current health risk assessment, we are using 

probabilistic E-R relationships based on analysis of individual data that describe the relationship 

between measures of personal exposure to O3 and measures of lung function recorded in the 

studies. Therefore, a risk assessment based on exposure-response relationships derived from 

controlled human exposure study data requires estimates of personal exposure to ambient O3. 

Because data on personal hourly exposures to O3 of ambient origin are not available, estimates of 

personal exposures to varying ambient concentrations are derived through exposure modeling, as 

described in Chapter 5. 

While the quantitative risk assessment based on controlled human exposure studies 

addresses only lung function responses, it is important to note that other respiratory responses 

have been found to be related to O3 exposures in these types of studies, including increased lung 

inflammation, increased respiratory symptoms, increased airway responsiveness, and impaired 

host defenses. Sufficient information is not available to quantitatively model these other 

endpoints. Section 6.2 of the ISA provides a discussion of these additional health endpoints 
6-3 

which are an important part of the overall characterization of risks associated with ambient O3

exposures. 

6.1.2 Comparison of Controlled Human Exposure- and Epidemiologic-based Risk 

Assessments 

In contrast to the exposure-response (E-R) relationships derived from controlled human 

exposure studies, epidemiological studies provide estimated concentration-response (C-R) 

relationships based on data collected in real world community settings. The assessment of health 

risk based on epidemiological studies is the subject of Chapter 7. The characteristics that are 

relevant to carrying out a risk assessment based on controlled human exposure studies versus one 

based on epidemiology studies can be summarized as follows: 

 The relevant controlled human exposure studies in the ISA provide data that can be used 

to estimate E-R functions, and therefore a risk assessment based on these studies requires 

as input (modeled) personal exposures to ambient O3. The relevant epidemiological 

studies in the ISA provide C-R functions, and, therefore, a risk assessment based on these 

studies requires as input (actual monitored or adjusted based on monitored) ambient O3 

concentrations, and personal exposures are not required as inputs to the assessment. 

 Epidemiological studies are carried out in specific real world locations (e.g., specific 

urban areas). To minimize extrapolation uncertainty, a risk assessment based on 

epidemiological studies is best performed in locations where the studies took place. 

Controlled human exposure studies, carried out in laboratory settings, are generally not 

specific to any particular real world location. A risk assessment based on controlled 

human exposure studies can therefore appropriately be carried out for any location for 

which there are adequate air quality and other data on which to base the modeling of 

personal exposures. 

 To derive estimates of risk from C-R relationships estimated in epidemiological studies, 

it is usually necessary to have estimates of the baseline incidences of the health effects 

involved. Such baseline incidence estimates are not needed in a controlled human 

exposure studies-based risk assessment. 

 Widely accepted ethical standards preclude the use of infants and young children in 

controlled human exposure studies, leaving a number of the most susceptible lifestages 

effectively unstudied under laboratory conditions. Similarly, other susceptible groups, 

such as people with lung disease, are not often participants in controlled human exposure 

studies. In contrast, epidemiology studies are able to include all lifestages and groups in a 

population or focus on a particular at-risk group. 
6-4 

6.2 SCOPE OF LUNG FUNCTION HEALTH RISK ASSESSMENT 

 The current controlled human exposure-based O3 health risk assessment is one approach 

used to estimate risks associated with exposure to ambient O3 in a number of urban study areas 

selected to illustrate the public health impacts of this pollutant. The short-term exposure related 

health endpoints selected for this portion of the O3 health risk assessment include those for which 

the ISA concludes that the evidence as a whole supports the general conclusion that O3, acting 

alone and/or in combination with other components in the ambient air pollution mix is causal or 

likely to be causally related to the endpoint. 

In the 2007 O3 NAAQS review, the controlled human exposure-based health risk 

assessment involved developing risk estimates for lung function decrements (≥ 10, ≥ 15, and 

≥ 20% changes in FEV1) in school-aged children (ages 5 to 18 years old). The strong emphasis 

on children reflects the finding of previous O3 NAAQS reviews that children are an important atrisk group. Due to the increased amount of time spent outdoors engaged in relatively high levels 

of physical activity (which increases intake), school-aged children as a group are particularly at 

risk for experiencing O3-related health effects. 

 Outdoor workers and other adults who engage in moderate exertion for prolonged 

periods or heavy exertion for shorter periods during the day also are clearly at risk for 

experiencing similar lung function responses when exposed to elevated ambient O3

concentrations. In this HREA, we focus the quantitative risk assessment for lung function 

decrements on all and asthmatic school-aged children (ages 5-18), and the adult population (ages 

19 and above). 

 For this assessment, lung function risks are estimated for 15 urban study areas, Atlanta, 

Baltimore, Boston, Chicago, Cleveland, Dallas, Denver, Detroit, Houston, Los Angeles, New 

York, Philadelphia, Sacramento, St. Louis, and Washington, DC. 

6.2.1 Selection of Health Endpoints 

The ISA identifies several responses to short-term O3 exposure that have been evaluated 

in controlled human exposure studies (U.S. EPA, 2013, sections 6.2.1.1, 6.2.2.1, 6.2.3.1, and 

6.3.1). These include decreased inspiratory capacity; decreased forced vital capacity (FVC) and 

forced expiratory volume in one second (FEV1); mild bronchoconstriction; rapid, shallow 

breathing patterns during exercise; symptoms of cough and pain on deep inspiration (PDI); 

increased airway responsiveness; and pulmonary inflammation. Such studies provide direct 

evidence of relationships between short-term O3 exposure and an array of respiratory-related 

effects, however, there are only sufficient E-R data at different concentrations to develop 

quantitative risk estimates for O3-related decrements in FEV1. Other responses to O3 which may 

be equally or more important than FEV1 decrements (e.g., inflammation) do not necessarily 
6-5 

correlate with FEV1 responses (ISA, section 6.2.3.1) and this risk assessment is not able to 

address these other responses. 

As stated in the 2006 Criteria Document (Table 8-3, p.8-68) for adults with lung disease, 

even moderate functional responses (e.g., FEV1 decrements ≥ 10% but < 20%) would likely 

interfere with normal activities for many individuals, and would likely result in more frequent 

medication use. In a letter to the Administrator, the CASAC O3 Panel stated that “'Clinically 

relevant' effects are decrements > 10%, a decrease in lung function considered clinically relevant 

by the American Thoracic Society” (Samet, 2011, p.2). The CASAC O3 Panel also stated that: 

a 10% decrement in FEV1 can lead to respiratory symptoms, especially in 

individuals with pre-existing pulmonary or cardiac disease. For example, 

people with chronic obstructive pulmonary disease have decreased ventilatory 

reserve (i.e., decreased baseline FEV1) such that a ≥ 10% decrement could 

lead to moderate to severe respiratory symptoms (Samet, 2011, p.7). 

This is consistent with the most recent official statement of the American Thoracic Society on 

what constitutes an adverse lung function health effect of air pollution: 

The committee recommends that a small, transient loss of lung function, by 

itself, should not automatically be designated as adverse. In drawing the 

distinction between adverse and nonadverse reversible effects, this committee 

recommended that reversible loss of lung function in combination with the 

presence of symptoms should be considered adverse (ATS, 2000, p.672). 

For this lung function risk assessment, a focus on the mid- to upper-end of the range of 

moderate levels of functional responses and higher (FEV1 decrements ≥ 15%) is appropriate for 

estimating potentially adverse lung function decrements in active healthy adults, while for people 

with asthma or lung disease, a focus on moderate functional responses (FEV1 decrements down 

to 10%) may be appropriate. 

6.2.2 Approach for Estimating Health Risk Based on Controlled Human Exposure 

Studies 

The major components of the health risk assessment based on data from controlled 

human exposure studies are illustrated in Figure 3-3 in Chapter 3. As shown in this figure, under 

this portion of the risk assessment, exposure estimates for a number of different air quality 

scenarios (i.e., recent year of air quality, just meeting the existing 8-hr and alternative standards) 

are combined with probabilistic E-R relationships derived from the controlled human exposure 

studies to develop risk estimates associated with recent air quality and after simulating just 

meeting the existing and alternative standards. The health effect included in this portion of the 

risk assessment is lung function decrement, as measured by changes in FEV1. The population 
6-6 

risk estimates for a given lung function decrement (e.g., ≥ 15% reduction in FEV1) are estimates 

of the expected number of people who will experience that lung function decrement, the number 

of times that people experience repeated occurrences of given lung function decrements, and the 

number of occurrences (person-days) of the given lung function decrement. The air quality and 

exposure analysis components that are integral to this portion of the risk assessment are 

discussed in Chapters 4 and 5. 

We used two approaches to estimate health risk. As done for the risk assessment 

conducted during the previous O3 NAAQS review, a Bayesian Markov Chain Monte Carlo 

approach was used to develop probabilistic E-R functions. These functions were then applied to 

the APEX estimated population distribution of 8-hr maximum exposures for people at or above 

moderate exertion (≥ 13 L/min-m2

 body surface area) to estimate the number of people expected 

to experience lung function decrements. The primary approach, based on the McDonnellStewart-Smith (MSS) FEV1 model, uses the time-series of O3 exposure and corresponding 

ventilation rates for each APEX simulated individual to estimate their personal time-series of 

FEV1 reductions, selecting the daily maximum reduction for each person. A key difference 

between these approaches is that the previous method estimates a population distribution of 

FEV1 reductions, where the MSS model estimates FEV1 reductions at the individual level. Each 

of these approaches is discussed in detail below. 

6.2.3 Controlled Human Exposure Studies 

Modeling of risks of lung function decrements as a function of exposures to O3 is based 

on application of results from controlled human exposure studies. As discussed in Chapter 6 of 

the ISA (U.S. EPA, 2013), there is a significant body of controlled human exposure studies 

reporting lung function decrements and respiratory symptoms in adults associated with 1- to 8-hr 

exposures to O3. In the ISA sections on controlled human exposure (Sections 6.2.1.1, 6.2.2.1, 

6.2.3.1, and 6.3.1) over 140 references to human clinical studies are reported. 

6.2.3.1 Lifestages 

Consistent with the approach used in the previous O3 NAAQS review and lacking a 

significant body of controlled human exposure studies on children, we judge that it is reasonable 

to estimate E-R relationships for lung function decrements associated with O3 exposures in 

children 5-18 years old based on data from young adult subjects (18-35 years old). As discussed 

in the ISA (U.S. EPA, 2013), findings from clinical studies for children and summer camp field 

studies of children 7-17 years old in at least six different locations in the U.S. and Canada found 

lung function decrements in healthy children similar to those observed in healthy young adults 

exposed to O3 under controlled chamber conditions. There are fewer studies of young children 
6-7 

than adolescents to draw upon, which may add to uncertainties in the modeling. Additional 

uncertainties are likely introduced since the lungs and airways of children are developing, while 

development is complete in adults (Dietert et al., 2000). The primary period of alveolar 

development is from birth to around eight years of age, but there is evidence for continued 

development through adolescence. The adult number of alveoli is reached by 2–3 years of age 

and the size and surface area of the alveoli increase until after adolescence (Hislop, 2002; 

Narayanan et al., 2012). Since it is unlikely that there will ever be a significant body of 

controlled human exposure studies on children (for ethical reasons), it may be that the best way 

to collect data on children’s lung function response to O3 is through summer camp studies, where 

children wear personal continuous 5-minute O3 monitors and have periodic lung function tests, 

with some method for estimating continuous ventilation rates. 

Lung function responses to O3 exposure for adults older than 18 decrease with age until 

around age 55, when responses are minimal. “Children, adolescents, and young adults appear, on 

average, to have nearly equivalent spirometric responses to O3, but have greater responses than 

middle-aged and older adults when similarly exposed to O3” (ISA p. 6-21). “In healthy 

individuals, the fastest rate of decline in O3 responsiveness appears between the ages of 18 and 

35 years (Passannante et al., 1998; Seal et al., 1996), more so for females than males (Hazucha et 

al., 2003). During the middle age period (35-55 years), O3 sensitivity continues to decline, but at 

a much lower rate. Beyond this age (>55 years), acute O3 exposure elicits minimal spirometric 

changes” (ISA p. 6-23). 

6.2.3.2 Asthma 

There have been several controlled human exposure studies of the effects of O3 on 

asthmatic subjects, going back to 1978 (Linn et al., 1978). In reference to these studies, the ISA 

states that “[b]ased on studies reviewed in the 1996 and 2006 O3 AQCDs, asthmatic subjects 

appear to be at least as sensitive to acute effects of O3 as healthy nonasthmatic subjects” (ISA p. 

6-20). Studies published since the 2006 O3 AQCD do not alter this conclusion (ISA, p. 6-20 to 6-

21). In the 2010 O3 NAAQS proposal (75 FR 2969-2972), EPA describes the evidence that 

people with asthma are as sensitive as, if not more sensitive than, normal subjects in manifesting 

O3-induced pulmonary function decrements. 

In reference to epidemiologic studies, the ISA states that “[t]he evidence supporting 

associations between short-term increases in ambient O3 concentration and increases in 

respiratory symptoms in children with asthma is derived mostly from examination of 1-h max, 

8-h max, or 8-h avg O3 concentrations and a large body of single-region or single-city studies. 

The few available U.S. multicity studies produced less consistent associations.” (ISA, p. 6-101 to 

6-102). “Although recent studies contributed mixed evidence, the collective body of evidence 
6-8 

supports associations between increases in ambient O3 concentration and increased asthma 

medication use in children” (ISA, p. 6-109). 

6.2.3.3 Ethnicity 

There are two controlled human exposure studies that have assessed differences in lung 

function responses comparing ethnic groups (ISA, p. 6-23 to 6-24). Both of these studies show 

greater FEV1 decrements in blacks than whites, however, epidemiologic studies were less 

supportive of this difference in response. The data available are insufficient to quantify any 

differences that might exist, due to the limited number of studies and a lack of consistency 

between disciplines. 

6.2.3.4 Body mass index 

Some studies have found greater FEV1 decrements to be associated with increasing BMI. 

BMI was included in some of the models of McDonnell et al. (2012); however, the BMI terms 

were found to be statistically insignificant, indicating that the effect of BMI on FEV1 in the 

presence of O3 is likely to be small, within the range of BMIs of the subjects studied. 

6.2.3.5 Outdoor workers 

Although there are no controlled human exposure studies that have had specifically 

outdoor workers as subjects, the studies are applicable to outdoor workers: the 6.6-hour 

experimental protocol was intended to simulate the performance of heavy physical labor for a 

full workday (ISA, p. 6-9). 

6.2.3.6 Variability of responses 

Responses to O3 exposure are variable within the population, even within cohorts of 

similar people (e.g., healthy young adult white males) (ISA, p. 6-16 to 6-20). Factors which 

contribute to interindividual variability include health status, body mass index, age, sex, 

race/ethnicity, and the intrinsic responsiveness of individuals. Other factors which contribute to 

the variability of responses include the duration and concentration of O3 exposure, the level of 

exercise and breathing rate, attenuation due to repeated exposures, and co-exposures with other 

pollutants. For specific individuals, lung function responses tend to be reproducible over a period 

of several months. 

6.2.3.7 Effects of altitude 

The controlled human exposure studies drawn upon for this lung function risk assessment 

were conducted at low altitudes (< 600 feet). It is not known whether it is more appropriate to 

use a mass concentration (μg/m3

) or a mixing ratio concentration (ppm) at higher altitudes where 
6-9 

the barometric pressure is lower. The E-R relationships used in the HREA are based on mixing 

ratio concentrations. If in fact mass concentrations are the appropriate exposure metric, then the 

lung function responses in a high-altitude city such as Denver (5300 feet asl1) could be 

overestimated by about 15%. 

A known effect of altitude is that people must breathe more rapidly to maintain their 

oxygen intake with increasing altitude (Bittar, 2002). This is not accounted for in the model of 

ventilation rates in APEX. 

6.2.4 The McDonnell-Stewart-Smith (MSS) Model 

In this review, EPA is investigating the use of a new model that estimates FEV1

responses for individuals associated with short-term exposures to O3 (McDonnell, Stewart, and 

Smith, 2007; McDonnell, Stewart, and Smith, 2010; McDonnell et al., 2012). This is a 

fundamentally different approach than the previous approach, for which the E-R function is at a 

population level, not an individual level. This model was developed using controlled human 

exposure data from studies using different exposure durations and different exertion levels and 

breathing rates. These data were from 15 controlled human O3 exposure studies that included 

exposure of 541 volunteers (ages 18 to 352) on a total of 864 occasions. These data are described 

in McDonnell et al. (1997). Schelegle et al. (2009) found that there appears to be a delay in 

response when modeling FEV1 decrements as a function of accumulated dose and estimated a 

threshold associated with the delay. McDonnell et al. (2012) refit their 2010 model using data 

from eight additional studies with 201 subjects and incorporating a threshold parameter into the 

model. Their threshold parameter allows for modeling a delay in response until accumulated 

dose (taking into account decreases over time according to first order reaction kinetics) reaches a 

threshold value and is found by McDonnell et al. (2012) to slightly improve model fit. That latest 

model is the model described here and is the model used in this risk assessment. The threshold is 

not a concentration threshold and does not preclude responses at low concentration exposures. 

Schelegle et al. (2012) have also developed a 2-compartment model for predicting FEV1

decrements (ISA, p. 6-15,16). Their model is similar to the MSS model in that it accounts for the 

effects of accumulated dose coupled with an exponential decay and also has a threshold, below 

which response is delayed. The primary difference between this model and the MSS model is 

that in the Schelegle et al. model the net accumulated dose is multiplied by an individual's 

responsiveness coefficient to obtain a predicted FEV1 decrement, whereas in the MSS model the 

FEV1 decrement increases as a sigmoid-shaped function of the net accumulated dose. Also, the 

 

1

 The average height of the O3 monitors in the city of Denver. 2

 The ages in these studies range from 18 years 1 month to 35 years 1 month. 
6-10 

Schelegle et al. model’s threshold is based on accumulated intake dose (the integral of 

concentration x volume inhaled), where the MSS model’s threshold is based on net accumulated 

dose (taking into account the first order decay). A direct comparison of the results of these two 

models has not been performed. 

The MSS model is conceptually a two-compartment model. The accumulated amount of 

exposure to O3 (exposure concentration times ventilation rate, loosely speaking a measure of 

dose) is modeled in the first compartment and modified by an exponential decay factor to yield 

an intermediate quantity X. The response (lung function decrement) of the individual to X is 

modeled in the second compartment (Figure 6-1). The threshold parameter imposes the 

constraint that there is no response while the value of X is below the threshold value. 

Figure 6-1. Two-Compartment Model 

C is exposure concentration, V is ventilation rate, t is time, X is an intermediate quantity, 

a is a decay constant. Adapted from Figure 1 in McDonnell et al. (1999). 

X is given by the solution of the differential equation (6-1): 

ࢄௗ

ௗ௧

ൌ ܥሺݐሻܸሺݐሻఉ଺ െ ߚହࢄሺݐሻ Equation (6-1)

X(t) increases with “dose” (C·Vβ6

) over time for an individual and allows for removal of 

O3 with a half-life of 1/β5 through the 2nd term in equation (6-1). In APEX, because the exposure 

concentration C(t), exertion level, and ventilation rate V(t) are constant over an event, this 

equation has an analytic solution for each event (“events” in APEX are intervals of constant 

activity and concentration, where an individual is in one microenvironment. Events range in 

duration from one to 60 minutes.): 

C(t)V(t)

dX/dt=C(t)V(t)‐aX

X(t)

aX (metabolism)

(dose)

logistic

response ΔFEV1

compartment 1 compartment 2
6-11 

ܺሺݐଵሻ ൌ ܺሺݐ଴ሻ݁ିఉହሺ௧ଵି௧଴ሻ ൅ ஼ሺ௧భሻ

ఉఱ

ܸሺݐଵሻఉ଺ሺ1 െ ݁ିఉହሺ௧ଵି௧଴ሻሻ Equation (6-2) 

C(t1) and V(t1) denote the (constant) values of C(t) and V(t) during the event from time t0

to time t1. 

This model calculates the FEV1 decrement due to O3 exposure (compartment 2) as: 

̅ܣ െ௜௞ ݃݁ܣଶሺߚ ൅ ଵߚሾ௎௜݁ ൌ௜௝௞ ܸ1ܧܨ∆%

ሻሿ ቄ ଵ

ଵାఉర௘షഁయࢀ೔ೕೖ െ ଵଵାఉర

ቅ൅ߝ ௞௝௜Equation (6-3) 

where Tijk = max{0, Xijk – β9}. β9 is a threshold parameter which allows X to increase up to the 

threshold before the median response is allowed to exceed zero. 

The variables in the above equations are defined as: 

The indices i,j,k refer to the i

th subject at the jth time for the kth experiment for that subject, 

C(t) is the O3 exposure concentration at time t (ppm) during the event, 

V(t) = VE(t)/BSA is the ventilation rate normalized by body surface area at time t 

 (L/min-m2), 

VE(t) is the expired minute volume at time t (L min-1), 

BSA is the body surface area (m2), 

t is the time (minutes), 

t0 is the time at the start of the event, t1 is the time at the end of the event, 

Ageik is age in years of the i

th subject in the kth study, 

Ā is an age parameter (taken to be the approximate mean age of the clinical study subjects in 

the McDonnell, Stewart, and Smith 2007 (Ā=25), 2010 (Ā=25), and 2012 (Ā=23.8) papers), 

Ui is a subject-level random effect (between-individual variability not otherwise captured by 

the model), and 

εijk is a variability term, which includes measurement error and within-individual variability 

not otherwise captured by the model. 

The values of the βs and the variances of the {Ui} and {εijk} were estimated from fits of 

the model to the data (see McDonnell, et al. (2007, 2010, and 2012) for details). In APEX, values 

of Ui and εijk are drawn from Gaussian distributions with mean zero and variances var(U) and 

var(ε), constrained to be within ±2 standard deviations from the means (when samples are 

outside of this range, they are discarded and resampled). The values of Ui are chosen once for 

each individual and remain constant for individuals throughout the simulation. The εijk are 

sampled daily for each individual. The best fit values (based on maximum likelihood) for these 

parameters are listed in Table 6-1. The values in parentheses are standard errors of the estimates 

(given here to two significant digits; the values in the papers are given to up to five significant 

digits). Although some of the parameters are quite different in the three models in Table 6-1, the 
6-12 

predictions of these three models are similar. The relative influences of the parameters are 

discussed in Section 6.5.1. 

Table 6-1. Estimated Parameters in the MSS Models. 

Model β1 β2 β3 β4 β5 β6 β9 var(U) var(E) 

20071, 

20102

9.9047 

(0.61) 

–0.4106 

(0.11) 

0.0164 

(0.0030) 

46.9397 

(7.3) 

0.003748

(0.00027)

0.9123 

(0.054) 

0.835 

(0.080) 

13.8279 

(0.36) 

20123 9.8057 

(0.74) 

–0.1907 

(0.28) 

0.01839 

(0.0051) 

65.826 

(12) 

0.003191

(0.00021)

0.8753 

(0.086) 0 0.9449 

(0.083) 

17.120 

(1.2) 

2012T4 10.916 

(0.84) 

–0.2104 

(0.31) 

0.01506 

(0.0033) 

13.497 

(4.7) 

0.003221

(0.00021)

0.8839 

(0.065) 

59.284 

(10) 

0.9373 

(0.082) 

17.0816 

(1.2) 

The values in parentheses are standard errors of the estimates. 1

 McDonnell, Stewart, and Smith (2007). Ā = 25. 2

 McDonnell, Stewart, and Smith (2010). Ā = 25. 3

 McDonnell, et al. (2012). Ā = 23.8. No-threshold. 4

 McDonnell, et al. (2012). Ā = 23.8. Threshold. 

We are using this model to estimate lung function decrements for people ages 5 and 

older. However this model was developed using only data from individuals aged 18 to 35 and the 

age adjustment term [β1 + β2 (Ageijk – Ā)] in the numerator of equation 6-3 is not appropriate for 

all ages. In addition to this age term, the effects of age are also taken into account through the 

dependence of ventilation rate and body surface area on age. The APEX estimates of lung 

function risk for different age groups are also influenced by the time spent outdoors and the 

activities engaged in by those groups, which vary by age (see Appendix 6E).

Clinical studies data for children which could be used to fit the model for children are not 

available at this time. In the absence of data, we are extending the model to ages 5 to 18 by 

holding the age term constant at the age 18 level. Since the response increases as age decreases 

in the range 18 to 35, this trend may extend into ages of children, in which case the responses of 

children could be underestimated. However, the slope of the age term in the MSS model is 

estimated based on data for ages 18 to 35 and does not capture differences in age trend within 

this range; in particular, we don’t know at what age the response peaks, which could be above or 

below 18. The evidence from clinical studies indicates that the responsiveness of children to O3

is about the same as for young adults (ISA, 2012, p. 6-21). This suggests that the age term for 

children should not be higher than the age term for young adults. See Sections 6.4.2 and 6.5.3, 

and Appendices 6D and 6E for more details. 

Because the responses to O3 decline from age 18 until around age 55 and for ages older 

than 55 the response are minimal, we let the age term for ages 35 to 55 linearly decrease to zero 

and set it to zero for ages > 55. 
6-13 

“In healthy individuals, the fastest rate of decline in O3 responsiveness 

appears between the ages of 18 and 35 years .... During the middle age period 

(35-55 years), O3 sensitivity continues to decline, but at a much lower rate. 

Beyond this age (>55 years), acute O3 exposure elicits minimal spirometric 

changes.” (ISA, 2012, p. 6-23) 

In order to extend the age term to ages outside the range of ages the MSS model is based 

on (ages 18-35), we reparameterize the age term in the numerator of equation 6-3 by 

[β1 + β2(α1 Age + α2)], for different ranges of ages (α1 and α2 depend on age), requiring that these 

terms match at each boundary to form a piecewise linear continuous function of age. The 

foregoing assumptions result in the following values of α1 and α2 for four age ranges (Table 6-2). 

Table 6-2. Age Term Parameters for Application of the 2012 MSS 

Threshold Model to All Ages. 

Age Range β1 β2 α1 α2

5 – 17 10.916 –0.2104 0 –5.8 

18 – 35 10.916 –0.2104 1 –23.8 

36 – 55 10.916 –0.2104 2.0341 –59.994 

> 55 0 0 0 0 

The lung function decrements estimated by the MSS (2010) model for a particular case 

are illustrated in Figure 6-2 and Figure 6-3. Figure 6-2 shows the predictions of the MSS model 

for 20-year old individuals with a (typical) body surface area (BSA) of 2 m2 and a target 

ventilation rate of 40 L/min (moderate exertion) and an O3 exposure level of 100 ppb, under the 

conditions of a typical 6.6-hour clinical study. Subjects alternated 50 minutes of moderate 

exercise with 10 minutes of rest for the first three hours, with the exercise occurring first. For the 

next 35 minutes (lunch), subjects continued exposure at rest. For the remaining three hours of the 

exposure period, subjects again alternated 50 minutes of exercise with 10 minutes of rest. The 

inter-individual variability predicted by this model is depicted by the boxplots in this figure. The 

predictions for the median individual over time are given by the line. Minute-by-minute 

predictions for the median individual for an exposure level of 100 ppb are shown in Figure 6-3. 

The stairstep response results from the pattern of exercise and rest during the experiment. 
6-14 

Figure 6-2. Distribution of Responses (Lung Function Decrements in FEV1) Predicted by 

the MSS Model for 20-Year Old Individuals. Exposure to 100 ppb O3 at Moderate Exercise 

(40 L/min, BSA=2 m2) Under the Conditions of a Typical 6.6-hour Clinical Study. 

The bottom and top edges of the boxes are at the 25th and 75th percentiles. The center horizontal line is 

drawn at the 50th percentile (median). The whiskers are at the 1st and 99th percentiles. FEV1 decrement (%)

-5

0

5

10

15

20

25

30

35

40

45

hour

01234567
6-15 

Figure 6-3. Median Response (Lung Function Decrements in FEV1) Predicted by the MSS 

Model for 20-Year Old Individuals. Exposure to 100 ppb O3 at Moderate Exercise (40 

L/min, BSA=2 m2) Under the Conditions of a Typical 6.6-hour Clinical Study. 

Figure 6-4 and Figure 6-5 illustrate the threshold effect based on McDonnell et al. (2012). 

Figure 6-4 is a graph of the median response for a population of 20-year old individuals over a 

6.6-hour time period. The exposure concentration is a constant 100 ppb over this time period, 

while the individuals are exercising (at 30 L/min-m2

 BSA) from hour 1 to hour 3 and at rest (5 

L/min-m2 BSA) otherwise. There is a 1.3-hour delay in response due to the threshold; without 

the threshold, the response starts increasing after exposure starts (hour 0). Figure 6-5 shows the 

corresponding probability of a response (FEV1 decrement) ≥ 10% over the time period for the 

two models. There is very little difference in response between the threshold and non-threshold 

models.FEV1 decrement (%)

0

1

2

3

4

5

6

7

hour

01234567
6-16 

Figure 6-4. Median Response (FEV1 Decrements) Predicted by the MSS Threshold and 

Non-Threshold Models for 20-Year Old Individuals, Constant 100 ppb O3 Exposure For 

6.6 Hours, 2 Hours Heavy Exercise From Hour 1 to 3 (30 L/min-m2 BSA). 

 

∆FEV1%

0

1

2

3

4

5

hour

01234567

Model no-threshold threshold
6-17 

Figure 6-5. Probability of Response ≥ 10% Predicted by the MSS Threshold and NonThreshold Models for 20-Year Old Individuals, Constant 100 ppb O3 Exposure For 6.6 

Hours, 2 Hours Heavy Exercise From Hour 1 to 3 (30 L/min-m2 BSA). 

6.2.5 The Exposure-Response Function Approach Used in Prior Reviews 

As described in section 3.1.2 of the 2007 Risk Assessment Technical Support Document 

(U.S. EPA, 2007b), a Bayesian Markov Chain Monte Carlo approach (Lunn et al., 2012) was 

used to estimate probabilistic E-R relationships for lung function decrements associated with 8-

hr O3 exposures occurring at moderate exertion. In the previous review, summary data from the 

Folinsbee et al. (1988), Horstman et al. (1990), McDonnell et al. (1991), and Adams (2002, 

2003, 2006) studies were combined to estimate E-R relationships for 8-hr exposures at moderate 

exertion for each of the three measures of lung function decrement (≥ 10, ≥ 15, ≥ 20% 

decrements in FEV1). In this HREA we have updated this E-R function with the results from two 

additional studies (Kim et al., 2011; Schelegle et al., 2009). The controlled human exposure 

study data were corrected on an individual basis for study effects in clean filtered air to remove 

any systemic bias that might be present in the data attributable to the effects of the study itself 

(e.g. exercise, diurnal effect, etc.) (ISA, Section 6.2.1.1). This is done by subtracting the FEV1

decrement in filtered air from the FEV1 decrement (at the same time point) during exposure to 

O3. An example of this calculation is given in Appendix 6D. 

Table 6-3 presents a summary of the study-specific results based on correcting all 

individual responses for the effect on lung function decrements of exercise in clean air. Probability of Response (%)

 0%

 2%

 4%

 6%

 8%

 10%

 12%

 14%

 16%

 18%

 20%

 22%

 24%

 26%

hour

01234567

Model no-threshold threshold
6-18 

Table 6-3. Study-specific O3 E-R Data for Lung Function Decrements Based on Correcting 

Individual Responses for the Effect on Lung Function of Exercise in Clean Air, Ages 18-35. 

Study, Grouped by 

Average O3

Exposure 

Protocol Number 

Exposed

Number of Responses 

∆FEV1 ≥

10% 

∆FEV1 ≥

15% 

∆FEV1 ≥

20% 

0.04 ppm O3

Adams et al. (2002) Square-wave, face mask 30 2 0 0 

Adams et al. (2006) Triangular 30 0 0 0 

0.06 ppm O3

Adams et al. (2006) 

Square-wave 30 2 0 0 

Triangular 30 2 2 0 

Kim et al. (2011) Square-wave 59 3 1 0 

Schelegle et al. (2009) Variable levels (0.06 ppm 

avg) 31 4 2 1 

0.07 ppm O3

Schelegle et al. (2009) Variable levels (0.07 ppm 

avg) 31 6 3 2 

0.08 ppm O3

Adams et al. (2002) Square-wave, face mask 30 6 5 2 

Adams et al. (2003) 

Square-wave, chamber 30 6 2 1 

Square-wave, face mask 30 5 2 2 

Variable levels (0.08 ppm 

avg), chamber 30 6 1 1 

Variable levels (0.08 ppm 

avg), face mask 30 5 1 1 

Adams et al. (2006) Square-wave 30 7 2 1 

Triangular 30 9 3 1 

F-H-M a Square-wave 60 17 11 8 

Kim et al. (2011) Square-wave 30 4 1 0 

Schelegle et al. (2009) Variable levels (0.08 ppm 

avg) 31 10 5 4 

0.087 ppm O3

Schelegle et al. (2009) Variable levels (0.087 ppm 

avg) 31 14 10 7 

0.1 ppm O3

F-H-M a Square-wave 32 13 11 6 

0.12 ppm O3

Adams et al. (2002) Square-wave, chamber 30 17 12 10 

Square-wave, face mask 30 21 13 7 

F-H-M a Square-wave 30 18 15 10 

a

 F-H-M combines data from Folinsbee et al. (1988), Horstman et al. (1990), and McDonnell et al. (1991).
6-19 

For the risk assessment conducted during the 2007 O3 NAAQS review (U.S. EPA, 

2007b), EPA considered both linear and logistic functional forms in estimating the E-R 

relationship and chose a 90 percent logistic/10 percent piecewise-linear split using a Bayesian 

Markov Chain Monte Carlo approach. This Bayesian estimation approach incorporates both 

model uncertainty and uncertainty due to sampling variability. 

For each of the three measures of lung function decrement, EPA assumed a 90 percent 

probability that the E-R function has the following 3-parameter logistic form:3

(1 )(1 )

(1 ) ( ; , , )   

  

     

  x

x

e e

e e

y x , Equation (6-4)

where x denotes the O3 concentration (in ppm) to which the individual is exposed, y 

denotes the corresponding response (decrement in FEV1 > 10%, > 15% or > 20%), and α, β, and 

γ are the three parameters whose values are estimated. 

We assumed a 10 percent probability that the E-R function has the following linear with 

threshold (hockey stick) form: 







 

    0, 0

, 0

( ; , ) for x

x for x

y x

 

   

  Equation (6-5) 

We assumed that the number of responses, S, out of N subjects exposed to a given 

concentration, x, has a binomial distribution with response probability given by Equation (6-4) 

with 90 percent probability and response probability given by Equation (6-5) with 10 percent 

probability. In the 2007 review, we also considered 80/20 and 50/50 probabilities for the logistic 

and hockey stick forms, and ran those as sensitivity analyses. We performed those analyses with 

the updated data and found that for each of the three E-R curves, the 90/10 mix has smaller error 

in fit (weighted RMSE) than the other two combinations of probabilities, and we are using only 

that function in this review. 

In some of the controlled human exposure studies, subjects were exposed to a given O3

concentration more than once – for example, using a constant (square-wave) exposure pattern in 

one protocol and a variable (triangular) exposure pattern in another protocol. However, because 

there were insufficient data to estimate subject-specific response probabilities, we assumed a 

single response probability (for a given definition of response) for all individuals and treated the 

repeated exposures for a single subject as independent exposures in the binomial distribution. 

 

3

 The 3-parameter logistic function is a special case of the 4-parameter logistic, in which the function is forced to go 

through the origin, so that the probability of response to 0.0 ppm is 0. 
6-20 

For each of the two functional forms (logistic and linear), we derived a Bayesian 

posterior distribution using this binomial likelihood function in combination with prior 

distributions for each of the unknown parameters (Box and Tiao, 1973). We assumed lognormal 

priors with maximum likelihood estimates of the means and variances for the parameters of the 

logistic function, and normal priors, similarly with maximum likelihood estimates for the means 

and variances, for the parameters of the linear function. For each of the two functional forms 

considered, we used 1,000 iterations as the “burn-in” period4

 followed by 9,000 iterations for the 

estimation. Each iteration corresponds to a set of values for the parameters of the (logistic or 

linear) E-R function. We combined the 9,000 sets of values from the logistic model runs with the 

last 1,000 sets of values from the linear model runs to get a single combined distribution of 

10,000 sets of values reflecting the 90 percent/10 percent assumption stated above. WinBUGS 

version 1.4.3 was used for these analyses (WinBUGS; Lunn et al., 2012). 

For any O3 concentration, x, we can derive the nth percentile response value, for any n, by 

evaluating the E-R function at x using each of the 10,000 sets of parameter values (9,000 of 

which were for a logistic model and 1,000 of which were for a linear model). The resulting 2.5th

percentile, median (50th percentile), and 97.5th percentile E-R functions for changes in FEV1 > 

10% are shown in Figure 6-6, along with the response data to which they were fit. The 

corresponding E-R functions for changes in FEV1 > 15% and > 20% are shown in Appendix 6A. 

The values of the functions are also provided in Appendix 6A. 

 

4

 Markov chain Monte Carlo (MCMC) simulations require an initial adaptive “burn-in” set of iterations, which are 

not used. This allows the MCMC sampling to stabilize. 
6-21 

Figure 6-6. Probabilistic E-R Relationships for FEV1 Decrements ≥ 10% for 8-hr 

Exposures At Moderate Exertion, Ages 18-35. Values associated with data points are the 

number of subject-exposures at each exposure concentration. 

The population risk is estimated by multiplying the expected risk by the number of 

people in the relevant population, as shown in Equation (6-6) below. The risk (i.e., expected 

fractional response rate) for the kth fractile, Rk is estimated as: 

1

( |)

N

k j kj

j

R P x RR e  Equation (6-6) 

where: 

ej = (the midpoint of) the j

th category of personal exposure to O3; 

Pj = the fraction of the population having personal exposures to O3 concentration 

 of ej ppm; 

k j RR | e = k-fractile response rate at O3 exposure concentration ej; 

N = number of intervals (categories) of O3 personal exposure concentration. 

0%

10%

20%

30%

40%

50%

60%

70%

80%

90%

0 0.02 0.04 0.06 0.08 0.1 0.12 0.14 0.16

Response Rate (%)

Ozone Exposure (ppm)

97.5th Pctl (FEV1≥10%)

Median (FEV1≥10%)

2.5th Pctl (FEV1≥10%)

Data for FEV1≥10%

60 150

31 331

32

31

90

Functional form mix:

90% logistic &

10% linear
6-22 

Exposure estimates used in this portion of the risk assessment were obtained from APEX 

for each of the 15 urban study areas and the five air quality scenarios. Chapter 5 provides 

additional details about the inputs and methodology used to estimate population exposure in the 

urban study areas. Exposure estimates for all and asthmatic school-aged children (ages 5 to 18) 

were combined with probabilistic E-R relationships for lung function decrements associated with 

8-hr exposure while engaged in moderate exertion. Individuals engaged in activities that resulted 

in an average equivalent (BSA-normalized) ventilation rate (EVR) for the 8-hr period at or above 

13 L/min-m2 BSA were included in the exposure estimates for 8-hr moderate or greater exertion. 

This range was selected based on the EVRs for the group of subjects in the controlled human 

exposure studies that were the basis for the E-R relationships used in this portion of the risk 

assessment. 

6.3 OZONE RISK ESTIMATES 

This section provides lung function risk estimates associated with several air quality 

scenarios: five recent years of air quality as represented by 2006 to 2010 monitoring data, and air 

quality in those years after simulating just meeting the existing O3 standard and alternative 

standard levels of 0.070, 0.065, and 0.060 ppm. The risk measures presented here are the 

percents of the population estimated to experience lung function responses greater than 10, 15, 

and 20%, one or more times or six or more times during an O3 season, for three age groups: 

school-aged children (ages 5-18), young adults (ages 19-35) and adults ages 36-55. Results for 

adults older than 55 are not presented since the responses for this age group are estimated to be 

minimal. People with multiple events with large lung function decreases are more at risk than 

those with only one such event during the O3 season. Although six events is less than once per 

month, we see dramatic decreases in population risk in going from one or more to six or more 

events during a season, which is why we report on six or more events rather than a higher 

number. 

In the figures and tables that follow, “base” indicates the base case scenario of recent air 

quality for the indicated year. “75,” “70,” “65,” and “60” respectively indicate the existing O3

standard and alternative standard levels of 0.070, 0.065, and 0.060 ppm. “75 6-8” indicates the 

0.075 ppm existing 8-hr standard based on rollback for the 2006-2008 period, while “75 8-10” 

indicates the existing standard scenario based on rollback for the 2008-2010 period. There are 

two estimates of results for the 2008 existing and alternative standard scenarios (because 2008 

overlaps the two rollback periods) and one for each of the other four years. These two estimates 

for 2008 can be quite different because of the relationship between the design value over the 

three-year period and the amount of adjustment to the air quality distribution in 2008 that can 

result. 
6-23 

6.3.1 Lung Function Risk Estimates Based on the McDonnell-Stewart-Smith Model 

Results based on the McDonnell-Stewart-Smith (2012) threshold model are summarized 

in this section; detailed results can be found in Appendix 6B. 

Figure 6-7 shows the results for school-aged children in the same format used in exposure 

results, explained in Section 5.3.1. Figure 6-7 depicts results for all urban study areas, year, and 

scenarios for ages 5 to 18 with ≥ 1 occurrences of FEV1 decrements ≥ 10, 15, 20% and illustrates 

the variation of results across study area, year, and scenarios. 

Figure 6-8 shows the variation across study areas (horizontally) and years (vertically) for 

the percent of school-aged children with ≥ 1 occurrences of FEV1 decrements ≥ 10% with air 

quality just meeting the potential alternative standard of 0.07 ppm. The points above each study 

area on this graph represent the risk for the six years for the study area (2008 has two points, 

corresponding to the different 2006-2008 and 2008-2010 design values used to adjust the air 

quality to meet 0.07 ppm). There is substantial variability both across years and across study 

areas. Denver has the highest overall risks, while Cleveland and New York have the lowest. Los 

Angeles has the smallest variation across years, with a range of 2.3% (from 14.3% to 16.6%). 

The other study areas have a range of around 4% to 7.5% across years. 

Table 6-4 and Table 6-5 present summary results (ranges over study areas and years) of 

FEV1 decrements ≥ 10 and 15% estimated by the MSS model for the different age groups. The 

results for asthmatic school-aged children are very similar to the results for all school-aged 

children and are not presented here. 
6-24 

Figure 6-7. Risk Results For All School-Aged Children With ≥ 1 Occurrences of FEV1

Decrements ≥ 10, 15, 20% For All Study Areas, Year, and Scenarios (y-axis is percent of children 

affected). Percent of school-aged children with 

≥ 1 occurrence of FEV1 decrements 

≥ 10% 
6-25 

Figure 6-8. Risk Results For All School-Aged Children With ≥ 1 Occurrences of FEV1

Decrements ≥ 10% Under The 0.07 ppm Alternative Standard Showing Variability Across 

Study Areas (Horizontally) and Years (Vertically). 

 

Percent of population

 8%

 9%

 10%

 11%

 12%

 13%

 14%

 15%

 16%

 17%

 18%

 19%

 20%

 21%

Urban area

A

t

l

a

n

t

a

B

a

l

t

i

m

o

r

e

B

o

s

t

o

n

C

h

i

c

a

g

o

C

l

e

v

e

l

a

n

d

D

a

l

l

a

s

D

e

n

v

e

r

D

e

t

r

o

i

t

H

o

u

s

t

o

n

L

o

s

A

n

g

e

l

e

s

N

e

w

Y

o

r

k

P

h

i

l

a

d

e

l

p

h

i

a

S

a

c

r

a

m

e

n

t

o

S

t

L

o

u

i

s

W

a

s

h

i

n

g

t

o

n
6-26 

Table 6-4. Ranges of Percents of Population Experiencing One or More and Six or More 

Days during the O3 Season with Lung Function Decrement (∆FEV1) More than 10%. The 

numbers in this table are the minimum and maximum percents estimated over all study 

areas and years, for each age group and scenario. 

Percent of People Experiencing ≥

1 day with ∆FEV1 ≥ 10% 

Percent of People Experiencing ≥

6 days with ∆FEV1 ≥ 10% 

Age group Scenario Minimum Maximum Minimum Maximum 

5 to 18 base 11% 31% 1% 9% 

5 to 18 75 11% 22% 1% 6% 

5 to 18 70 8% 20% 1% 5% 

5 to 18 65 2% 18% 0% 4% 

5 to 18 60 4% 13% 0% 3% 

19 to 35 base 3% 13% 0% 1% 

19 to 35 75 3% 9% 0% 1% 

19 to 35 70 2% 8% 0% 1% 

19 to 35 65 1% 6% 0% 1% 

19 to 35 60 1% 5% 0% 0% 

36 to 55 base 1% 4% 0% 0% 

36 to 55 75 1% 2% 0% 0% 

36 to 55 70 0% 2% 0% 0% 

36 to 55 65 0% 2% 0% 0% 

36 to 55 60 0% 1% 0% 0% 

> 55 All 0% 0% 0% 0% 

 
6-27 

Table 6-5. Ranges of Percents of Population Experiencing One or More and Six or more 

Days during the O3 Season with Lung Function Decrement (∆FEV1) More than 15%. The 

numbers in this table are the minimum and maximum percents estimated over all study 

areas and years, for each age group and scenario. 

Percent of People Experiencing ≥

1 day with ∆FEV1 ≥ 15% 

Percent of People Experiencing ≥

6 days with ∆FEV1 ≥ 15% 

Age group Scenario Minimum Maximum Minimum Maximum 

5 to 18 base 2% 12% 0% 3% 

5 to 18 75 2% 6% 0% 1% 

5 to 18 70 2% 5% 0% 1% 

5 to 18 65 0% 4% 0% 1% 

5 to 18 60 0% 3% 0% 0% 

19 to 35 base 0% 3% 0% 0% 

19 to 35 75 0% 2% 0% 0% 

19 to 35 70 0% 1% 0% 0% 

19 to 35 65 0% 1% 0% 0% 

19 to 35 60 0% 1% 0% 0% 

36 to 55 base 0% 1% 0% 0% 

36 to 55 75 0% 0% 0% 0% 

36 to 55 70 0% 0% 0% 0% 

36 to 55 65 0% 0% 0% 0% 

36 to 55 60 0% 0% 0% 0% 

> 55 All 0% 0% 0% 0% 

Figure 6-9 illustrates the distribution of responses (FEV1 decrements > 10%) across 

ranges of ambient concentrations of O3 for school-aged children for one city and scenario (Los 

Angeles, 2006 recent air quality). The concentrations are daily 8-hr average ambient 

concentrations during the 8-hr period with maximum 8-hr average exposure for that day. 

These concentrations are less than but close to daily maximum 8-hr average ambient 

concentrations and are greater than daily maximum 8-hr average exposure concentrations. The 

percents in this chart reflect the frequencies of person-days with FEV1 decrements ≥ 10% within 

a concentration bin as percents of all person-days with FEV1 decrements ≥ 10%. Figure 6-9 

shows that more than 90% of daily instances of FEV1 decrements ≥ 10% occur when 8-hr 

average ambient concentrations are above 40 ppb for this modeled scenario. This distribution 

will be different for different study areas, years, and air quality scenarios. 
6-28 

Figure 6-9. Distribution of Daily FEV1 Decrements ≥ 10% Across Ranges of 8-hr Average 

Ambient O3 Concentrations (Los Angeles, 2006 recent air quality). 

Outdoor Workers 

Outdoor workers spend more time outdoors than the general population and therefore are 

at higher risk for health effects due to O3. We conducted simulations of outdoor workers ages 19-

35 for Atlanta (2006) for the existing and alternative standards to estimate the risk of this group 

for experiencing FEV1 decrements ≥ 15%. The methodology for simulating outdoor workers 

involves modifying activity diaries to represent outdoor workers and is described in Section 5.3.3 

in Chapter 5. Table 6-6 shows the results of these simulations and compares them with the 

results for the general population, ages 19-35. The percents of people experiencing one or more 

FEV1 decrements ≥ 15% during the 2006 O3 season in Atlanta are 3.6 times higher for outdoor 

workers than for the general population (ages 19-35) under the existing standard, and range up to 

5.3 times higher for the alternative standards. The percents of people experiencing six or more 

FEV1 decrements ≥ 15% during the 2006 O3 season in Atlanta are 24 times higher for outdoor 

workers than for the general population under the existing standard, and range up to 150 times 

higher for the alternative standards. As expected, we see that the risk of repeated occurrences of Frequency of responses (percent)

0

2

4

6

8

10

12

14

16

18

20

8-hour average concentration (ppb)

0-5

5-10

10-20

20-30

30-4040-5050-6060-7070-8080-90

90-100

100-110

110-120

> 120
6-29 

FEV1 decrements ≥ 15% is much greater for outdoor workers than for the general population. 

Part of the reason for this is that APEX tends to underestimate the number of individuals who 

have very repetitive activity patterns (e.g., 9 to 5 weekdays office workers) when using the 

CHAD activity database and the method selected for generating longitudinal diary profiles (see 

Section 5.3.1). 

Table 6-6. Percents of the General Population and Outdoor Workers (ages 19-35) 

Experiencing One or More and Six or More FEV1 Decrements ≥ 15% (based on Atlanta 

2006 APEX simulations). 

Scenario 

General 

population 

ages 19-35 

Outdoor workers 

ages 19-35 

1 or more occurrences 

Existing standard 1.2% 4.3% 

70 ppb alt. std. 0.84% 3.2% 

65 ppb alt. std. 0.55% 2.5% 

60 ppb alt. std. 0.32% 1.7% 

6 or more occurrences 

Existing standard 0.05% 1.2% 

70 ppb alt. std. 0.018% 0.93% 

65 ppb alt. std. 0.005% 0.74% 

60 ppb alt. std. 0.005% 0.55% 

6.3.2 Lung Function Risk Estimates Based on the Exposure-Response Functions 

Approach Used in Prior Reviews 

In this section we present lung function risk estimates for all school-aged children 

following the methodology used in previous reviews, based on updated E-R functions. In 

Appendix 6C we compare these estimates with those from the previous review. Table 6-7 

provides an overall summary of results for each air quality scenario by tabulating the minimum 

and maximum estimates over all study areas and years of percents of all school-aged children 

(ages 5 to 18) experiencing one or more days (during the O3 season) with FEV1 decrement more 

than 10 and 15%. This table can be compared with Table 6-4 and Table 6-5, which have 

analogous results for the MSS model. These results are much lower than the MSS model results. 

The reasons for this are described in Section 6.3.3 below. 
6-30 

Table 6-7. Ranges of Percents of all School-aged Children Experiencing One or More Days 

during the O3 Season with Lung Function Decrement (∆FEV1) More than 10 and 15%, 

based on the E-R Function Approach. The numbers in this table are the minimum and 

maximum percents estimated over all study areas and years. 

Scenario 

minimum 

percent 

experiencing 

≥ 1 day with 

∆ FEV1 ≥ 10% 

maximum 

percent 

experiencing

≥ 1 day with 

∆ FEV1 ≥ 10% 

minimum 

percent 

experiencing

≥ 1 day with 

∆ FEV1 ≥ 15% 

maximum 

percent 

experiencing 

≥ 1 day with 

∆ FEV1 ≥ 15% 

base 4% 11% 1% 5% 

75 3% 6% 1% 2% 

70 3% 6% 1% 2% 

65 1% 5% 0% 1% 

60 2% 3% 0% 1% 

6.3.3 Comparison of the MSS Model with the Exposure-Response Function Approach 

There are two key differences between the MSS and E-R models. The E-R model 

estimates the distribution of FEV1 decrements across the population or study group, whereas the 

MSS model estimates FEV1 decrements at the individual level and then these are aggregated to 

obtain the population distribution. Thus the MSS model allows for detailed analyses of 

conditions that influence risk. Second, the E-R model estimates FEV1 decrements only for 8-hr 

average exposures when the 8-hr average exertion level is moderate or greater. The MSS model 

estimates FEV1 decrements for any averaging time and therefore accounts for a wider range of 

activities that might result in FEV1 decrements. 

A comparison of the MSS model with the E-R function approach for the 2006 existing 

standard scenarios is summarized in Table 6-8 which lists estimates of the percents of schoolaged children estimated to experience lung function responses greater than 10, 15, and 20%. The 

MSS model estimates are significantly higher than the E-R function approach estimates. In most 

cases, the MSS model gives results about a factor of three higher than the E-R function model for 

school-aged children. This is expected, since, as discussed above, the MSS model includes 

responses for a wider range of exposure protocols (under different levels of exertion, lengths of 

exposures, and patterns of exposure concentrations) than the E-R model of previous reviews. 
6-31 

Table 6-8. Comparison of Responses from the MSS Model with Responses from the 

Population E-R Method, 2006 Existing Standard Air Quality Scenario, Ages 5 to 18. 

Urban Study 

Area 

≥ 10% FEV1 decrement ≥ 15% FEV1 decrement ≥ 20% FEV1 decrement 

MSS model E-R method MSS model E-R method MSS model E-R method

Atlanta 19.2% 5.6% 5.3% 1.7% 2.1% 0.7% 

Baltimore 18.6% 5.4% 5.2% 1.6% 2.1% 0.7% 

Boston 13.6% 4.5% 3.7% 1.2% 1.4% 0.5% 

Chicago 14.4% 4.7% 3.9% 1.3% 1.6% 0.5% 

Cleveland 13.5% 4.2% 3.3% 1.1% 1.2% 0.4% 

Dallas 21.6% 6.0% 6.4% 1.8% 2.7% 0.8% 

Denver 20.2% 5.8% 5.6% 1.7% 2.2% 0.7% 

Detroit 13.6% 4.4% 3.5% 1.2% 1.3% 0.4% 

Houston 16.2% 4.7% 4.2% 1.3% 1.6% 0.5% 

Los Angeles 18.2% 4.8% 4.2% 1.2% 1.5% 0.5% 

New York 12.7% 4.2% 3.2% 1.1% 1.2% 0.4% 

Philadelphia 16.4% 4.8% 4.2% 1.3% 1.6% 0.5% 

Sacramento 17.9% 5.1% 4.8% 1.4% 2.8% 0.6% 

St. Louis 18.6% 5.4% 5.1% 1.6% 2.0% 0.6% 

Washington 15.9% 4.6% 4.0% 1.3% 1.5% 0.5% 

Since the E-R method of the previous reviews only looks at 8-hr exposures concomitant 

with EVR ≥ 13 L/min-m2

 BSA (hereafter, EVR ≥ 13), it is of interest to compare the E-R method 

results with the corresponding MSS model results (instances of ∆FEV1 ≥ 10, 15, 20% 

concomitant with EVR ≥ 13). 

We performed this comparison for four APEX simulations: the Atlanta March 1-October 

30, 2006 base case, ages 18-35; the Los Angeles May 29-July 28, 2006 base case, age 25; the 

Los Angeles May 29-July 28, 2006 base case, ages 18-35; and the Los Angeles Jan 1-Dec 31, 

2006 base case, ages 18-35. 

For the Atlanta simulation, the E-R function approach gives 5.0, 1.8, and 0.9% 

responding for ∆FEV1 ≥ 10, 15, 20%. The MSS model approach gives 11.54, 3.26, and 1.28% 

responding for ∆FEV1 ≥ 10, 15, 20%. The percents of the population for ∆FEV1 ≥ 10, 15, 20% at 

the end of the daily max 8-hr average exposure period where the concomitant 8-hr average EVR 

is ≥ 13 are 6.67%, 2.09%, and 0.84%. 15.17% of the population never have any instances of 

EVR ≥ 13 and 0.41% have at least one occurrence of ∆FEV1 ≥ 10% while never having EVR ≥

13 for any 8-hr period. 4.46% (not among the 15.17%) have instances of ∆FEV1 ≥ 10% but none 

of those instances with concomitant EVR ≥ 13. The 11.54% responding is made up of 6.67% of 
6-32 

the population with instances of ∆FEV1 ≥ 10% concomitant with EVR ≥ 13 and 4.87% with 

instances of ∆FEV1 ≥ 10% not concomitant with EVR ≥ 13. 

Table 6-9 and Table 6-10 summarize the pertinent results for the Atlanta and three Los 

Angeles simulations. Looking at the first rows of these tables shows that these models have 

similar corresponding results. The broader scope of activity/exposure patterns encompassed by 

the MSS model, beyond the 8-hr average EVR ≥ 13 restriction of the E-R model, contributes 

from a third to a half to the total MSS model risk and to a large part explains the differences 

between the models for ages 18-35. The difference between the MSS and E-R models is larger 

for school-aged children than for adults ages 18-35 due to the increased EVR and time spent 

outdoors in children compared to adults. 
6-33 

Table 6-9. Comparison of MSS Model and E-R Model of Previous Reviews for Atlanta, Mar 1-Oct 30, 2006, 

Component of results MSS model ∆FEV1 ≥ 10% E-R model ∆FEV1 ≥ 10% MSS model ∆FEV1 ≥ 15% E-R model ∆FEV1 ≥ 15% M

∆F

profiles with instances of ∆FEV1 ≥ cutoff 

concomitant with 8-hr EVR ≥ 13 6.7% 5.0% 2.1% 1.8% 

profiles with instances of ∆FEV1 ≥ cutoff never 

concomitant with 8-hr EVR ≥ 13 4.8% 1.2% 

Final result of each model 11.5% 5.0% 3.3% 1.8% 

Table 6-10. Comparison of MSS Model and E-R Model of Previous Reviews for Los Angeles, Jan 1-Dec 31, 2

Component of results MSS model ∆FEV1 ≥ 10% E-R model ∆FEV1 ≥ 10% MSS model ∆FEV1 ≥ 15% E-R model ∆FEV1 ≥ 15% M

∆F

profiles with instances of ∆FEV1 ≥ cutoff 

concomitant with 8-hr EVR ≥ 13 7.9% 6.2% 2.6% 2.6% 

profiles with instances of ∆FEV1 ≥ cutoff never 

concomitant with 8-hr EVR ≥ 13 6.5% 1.8% 

Final result of each model 14.4% 6.2% 4.4% 2.6% 
6-34 

Figure 6-10 compares the E-R function to the response curve of the MSS model restricted 

to 8-hr average EVR ≥ 13 and shows that these curves are very close. The E-R model has a 

higher response for the low and high ranges of exposure concentrations, while the MSS model is 

higher in the mid-range of exposures. 

Figure 6-10. Comparison of E-R and MSS Model (restricted to 8-hr average EVR ≥ 13) 

Response Functions (Atlanta 2006 base case, ages 18-35). 

Another element of the difference between the models derives from the distribution of 

EVR in the clinical studies the E-R approach is based on and how this compares to the 

distribution of EVR in the APEX simulations. Most of the clinical studies are conducted with a 

target EVR of 20 L/min-m2

 BSA and the actual EVRs vary somewhat around this value. The 

rationale for the cutpoint of 13 L/min-m2

 BSA is described in EPA’s responses to comments on 

the 1996 proposed rule on the NAAQS for O3 (Federal Register, 1996) as “for the 8-hr health 

risk assessment the range (based on being within 2 standard deviations of the mean) of EVRs 

observed in the subjects who participated in the study [McDonnell et al., 1991] was 13-27 liters Response probability

 0%

 1%

 2%

 3%

 4%

 5%

 6%

 7%

 8%

 9%

 10%

 11%

 12%

 13%

 14%

 15%

 16%

 17%

 18%

 19%

 20%

 21%

 22%

 23%

 24%

Ozone exposure (ppb)

0 10 20 30 40 50 60 70 80

∆FEV1>=10% (MSS) ∆FEV1>=15% (MSS) ∆FEV1>=20% (MSS)

∆FEV1>=10% (E-R) ∆FEV1>=15% (E-R) ∆FEV1>=20% (E-R)
6-35 

per minute per meter squared [BSA] (L/min-m2).” Figure 6-11 shows the distribution of EVRs ≥

13 for the Atlanta simulation and is clearly shifted much lower than the distribution of EVR in 

the clinical studies. This could lead to an overestimation of the percent of responders by the E-R 

method, since higher EVRs lead to higher lung function decrements and it is applying an E-R 

function based on EVRs around 20 to a population with median EVRs around 14.5. 

Figure 6-11. Distribution of Daily Maximum 8-hr Average EVR For Values of EVR ≥ 13 

(L/min-m2

) (midpoints on vertical axis) (Atlanta 2006 base case, ages 18-35). 

 

PCT.

CUM.

PCT.

34.78 34.78

22.39 57.17

14.63 71.80

9.64 81.44

6.36 87.80

4.20 92.00

2.77 94.77

1.80 96.56

1.17 97.74

0.77 98.51

0.51 99.02

0.34 99.37

0.22 99.59

0.15 99.74

0.10 99.83

0.06 99.90

0.04 99.94

0.03 99.97

0.01 99.98

0.01 99.99

0.00 99.99

0.00 100.00

0.00 100.00

EVR

 35.5

 34.5

 33.5

 32.5

 31.5

 30.5

 29.5

 28.5

 27.5

 26.5

 25.5

 24.5

 23.5

 22.5

 21.5

 20.5

 19.5

 18.5

 17.5

 16.5

 15.5

 14.5

 13.5

FREQUENCY

0 200000 400000 600000 800000 1000000 1200000
6-36 

6.4 EVALUATION OF THE MSS MODEL 

6.4.1 Summary of Published Evaluations 

McDonnell et al. (2010) performed a detailed evaluation of their model using two 

methods: (1) cross-validation and (2) comparison of an independent data set against the 

predictions of the model. 

The cross-validation was based on the data set of 15 EPA studies from which their 

original model was developed (McDonnell et al., 2007). This data set has 541 subjects, each with 

multiple measurements during single experiments. Subjects were omitted from the data set, one 

at a time, the model refit to the reduced data set, and the resulting parameters used to predict the 

FEV1 decrements for the omitted subject. The authors then compare the mean predictions and 

mean observed values for each subject and presented these results in a scatter plot (Figure 1b, 

McDonnell et al., 2010). The observations exhibit much more variability than the predictions; for 

observed values of 20%, predicted values range from around 2 to 19%; and all observed values 

above 20% are underpredicted (the observed values range from -20 to 60%, while the predicted 

values range from 0 to 20%). These features result from the omission of the inter- and intraindividual variability terms (Ui and εijk) in the MSS model (equation 6-3), which are accounted 

for in the risk estimates in this chapter. 

Model predictions were compared against an independent data set of seven clinical 

studies with a total of 204 subjects (McDonnell et al., 2010). Graphs of predicted and observed 

study means vs. time show fair to good model fit. The authors do not present overall fit statistics 

that are directly commensurate with the statistics of interest in this risk assessment: the 

proportions of people with FEV1 decrements greater than 10, 15, and 20%. 

McDonnell et al. (2012) do compare observed and predicted proportions of people with 

FEV1 decrements greater than 10, 15, and 20% and provide the corresponding scatter plots 

(Figure 4). They find the model to be unbiased, with the slopes of the observed vs. predicted 

lines for 10, 15, and 20% to be around 1.0 and the R2

 respectively 0.78, 0.73, and 0.67. The 

higher observed proportions of people with FEV1 decrements greater than 10, 15, and 20% 

tended to be substantially underpredicted. 

6.4.2 Children 

A clinical study with children (ages 8-11; mean, 10 years; n=22), exposed to 120 ppb O3

over 2.5 hours at heavy exertion levels was done by McDonnell et al. (1985). This study could be 

used to fit the model for children if all of the measurements of FEV1 and ventilation rates were 

available. The paper lists the end-of exposure FEV1 responses for each individual (but not 

ventilation rates), which we use to compare with the MSS model with the age term extension 

described in Section 6.2.4. The numbers of subjects with clean-air adjusted responses greater 
6-37 

than 10%, 15%, and 20% are respectively 4, 2, and 1, corresponding to 18.2%, 9.1%, and 4.5% 

of the number of subjects. We ran the MSS 2010 model using the mean and standard deviation of 

the ventilation rates reported in the paper. Resting ventilation rates were assumed to be 10.4 

L/min (Avol et al., 1985) and BSA to be 1.08 m2

 (U.S. EPA, 2011). Details of this comparison 

can be found in Appendix 6D. 

Table 6-11 compares the results of this simulation with the results of McDonnell et al. 

(1985). The agreement is fairly good. Due to the limited sample size of 22 subjects from only 

one study and the assumptions made in running the MSS model, this does not provide 

confirmation that the age term extension is correct; on the other hand, this comparison does not 

indicate that there is a problem with the age term extension. Information is not available that 

would allow us to provide respectable confidence intervals for these estimates. 

Table 6-11. Comparison of Responses from the MSS 2010 Model with Responses from 

McDonnell et al. (1985). 

≥ 10% FEV1 decrement ≥ 15% FEV1 decrement ≥ 20% FEV1 decrement

MSS model McDonnell 

et al. (1985) MSS model McDonnell et al. (1985) MSS model McDonnell et al. (1985)

Percent 

responding 

18.4% 18.2% 

(4 subjects) 

6.8% 9.1% 

(2 subjects) 

2.3% 4.5% 

(1 subject) 

6.4.3 Threshold vs. Non-Threshold Models 

The difference between the results of the MSS threshold and non-threshold models is 

minor, with the threshold version estimates of lung function decrements almost identical to the 

no-threshold version for the Atlanta 2006 recent air quality base case, as can be seen by 

comparing Table 6-12 with Table 6-13, and inspection of Figures 6-4 and 6-5. This is consistent 

with the logistic form of the model, where the impact of exposures to low concentrations on risk 

is small. 
6-38 

Table 6-12. Percents of the Population by Age Group with One or More Days during the 

O3 Season with Lung Function (FEV1) Decrements more than 10, 15, and 20% (Atlanta 

2006 base case), MSS Threshold Model, Ambient Monitor Data.5

Age 

Group 

∆FEV1 ≥

10%

∆FEV1 ≥

15%

∆FEV1 ≥

20%

5 to 18 31% 13% 6.4%

19 to 35 11% 3.1% 1.3%

36 to 55 3.7% 0.60% 0.14%

Table 6-13. Percents of the Population by Age Group with One or More Days during the 

O3 Season with Lung Function (FEV1) Decrements more than 10, 15, and 20% (Atlanta 

2006 base case), MSS No-Threshold Model, Ambient Monitor Data. 

Age 

Group 

∆FEV1 ≥

10%

∆FEV1 ≥

15%

∆FEV1 ≥

20%

5 to 18 31% 13% 6.6%

19 to 35 11% 3.1% 1.3%

36 to 55 3.8% 0.60% 0.15%

6.5 CHARACTERIZATION OF UNCERTAINTY 

In the controlled human exposure study based risk assessment, there are two broad 

sources of uncertainty to the risk estimates. One of the most important sources of uncertainty is 

the estimation by APEX of the population distribution of individual time series of O3 exposures 

and ventilation rates. The uncertainty regarding these estimated exposures is discussed in 

Chapter 5; they are not discussed further here. 

 

5

 In the first draft HREA, monitor-level air quality was provided as input to the APEX model. As discussed in 

Chapter 5, tract-level air quality was used in APEX for this HREA. Monitor-level air quality is used for the APEX 

simulations here, since these simulations take less time to run. This does not affect the analyses here, since the two 

air quality formats yield very similar results (see Appendix 6F). 
6-39 

In this section, uncertainties associated with the second broad source of uncertainty in the 

risk calculation are discussed, namely, uncertainties in the lung function risk model. The specific 

sources of uncertainty covered are: 

 Statistical model form 

 Convergence of APEX results 

 Application of model for all lifestages 

 Application of model for asthmatic children 

 Interaction between O3 and other pollutants 

6.5.1 Statistical Model Form 

The MSS model is a 2-compartment model, the form of which is based on physical 

considerations. It accommodates these key features of human exposure studies: (1) FEV1

responses increase with increasing O3 concentration, ventilation rate, and duration of exposure if 

the other two variables are held constant, (2) the effect of each of these three variables depends 

on the levels of the other two variables, (3) FEV1 responses depend on age, (4) certain 

individuals are consistently more responsive to O3 exposure, and (5) O3–induced FEV1

decrements improve within a few hours of cessation of exposure (McDonnell et al., 2007). These 

considerations support the form of the model, as do model evaluations that have been performed 

(Section 6.4.1). Although the model does not have good predictive ability for individuals 

(psuedo-R2 0.28), it does better at predicting the proportion of individuals with FEV1 decrements 

≥ 10, 15, and 20% (psuedo-R2s of 0.78, 0.74, 0.68) (McDonnell et al., 2012). 

The clinical studies that these models’ estimates are based on were conducted with young 

adult volunteers rather than randomly selected individuals, so it may be that selection bias has 

influenced the model parameter estimates. 

The parameter estimates are not very precise, partly as the result of correlations between 

the parameter estimates. Table 6-14 gives 95 percent confidence intervals for each of the 

parameter estimates as percents of the estimates, based on the standard errors reported by 

McDonnell et al. (2012). Figure 6-12 shows how much the modeled number of children with one 

or more FEV1 decrements ≥ 10% changes when each parameter is increased by five percent 

(keeping the other parameters fixed at their estimates). The MSS model is also sensitive to the 

exposure concentrations, but we have not quantified that sensitivity. The scenario modeled is the 

Los Angeles 2006 recent conditions base case. The physiological parameter MET, a measure of 

the level of exertion for a given activity (see Appendix 6E), is also included here for comparison. 

MET is a key variable in calculating ventilation rates and is specified by a distribution for each 

activity. Here we have shifted all MET distributions by +5% of their means.
6-40 

Table 6-14. MSS Threshold Model Estimated Parameters with Confidence Intervals. 

β1 β2 β3 β4 β5 β6 β9 var(U) var(E) 

parameter 

estimate 

10.916 -0.2104 0.01506 13.497 0.003221 0.8839 59.284 0.9373 17.0816

standard 

error 

0.8446 0.31 0.00333 4.734 0.000207 0.0647 10.192 0.0824 1.1506 

95% conf. 

interval ±15% ±289% ±43% ±69% ±13% ±14% ±34% ±17% ±13% 

from McDonnell et al. (2012). 

The most influential parameter in Figure 6-12 is β6, the power to which ventilation rate is 

raised in the MSS model, which makes sense since inhaled dose is equal to the ventilation rate 

multiplied by the exposure. An increase of five percent in β6 leads to 27, 40, and 47 percent 

increases respectively in the modeled number of children with FEV1 decrements ≥ 10, 15 and 

20%. The next most influential parameter is the variance of E, the intra-individual variability 

term. The least influential parameter is β2, the slope of the age term. 

Since the MSS model parameter estimates are to some extent correlated, if we were to 

increase a parameter by five percent and hold it fixed while refitting the model, the remaining 

parameters would shift to compensate, and the sensitivity calculated from that model’s results 

would be much less than the corresponding sensitivity in Figure 6-12. As a result of this, the 

sensitivities in Figure 6-12 overestimate the sensitivities which account for parameter 

correlation. On the other hand, we are only increasing each parameter by five percent, which is 

much less than the 95% confidence intervals given in Table 6-14. The uncertainty in the risk 

estimates resulting from parameter uncertainty may be more or less than is indicated in Figure 

6-12. 

We are unable to properly estimate the true sensitivities or quantitatively assess the 

uncertainty of the MSS model, since all of the clinical data used by McDonnell and coworkers to 

fit the MSS model are not available to EPA (in particular, some studies by Adams and coworkers 

are not available to EPA). 

6.5.1.1 Age term significance 

As discussed in Section 6.5.3 below, there are uncertainties in extrapolating the MSS 

model down to age 5 from the age range of 18 to 35 to which the model was fit. Further 

considerations indicating that the uncertainty of the extension to children of the MSS model 

could be substantial are that the age coefficient β2 = −0.21 (s.e. 0.31) in the MSS model is not 

statistically significantly different from zero; and when the MSS model is fit to the U.C. Davis 

clinical data the age term is positive, β2 = +0.19 (0.60), although also not statistically 

significantly different from zero (McDonnell et al., 2012). Note that, in the previous section, β2 

was found to be the least influential model parameter.
6-41 

Figure 6-12. Sensitivity (Percent Change) of Population With One or More FEV1

Decrements ≥ 10% to a 5% Increase in Individual MSS Model Parameter Estimates. 
6-42 

6.5.1.2 The inter- and intra-individual variability terms U and ε

The MSS model has random variables for inter-individual (between-individual) 

variability (U) (ISA, p. 6-16) and intra-individual (within-individual) variability (ε) (see equation 

6-3). The variable U reflects the responsiveness of an individual to O3 and each individual 

simulated in APEX is assigned a value of U drawn from a Gaussian distribution with mean zero 

and variance estimated when fitting the MSS model. In order to estimate Var(U), it is necessary 

to have repeated clinical trials using the same individuals. There are few of these in the data used 

to fit the MSS model, making it harder to reliably estimate Var(U). Furthermore, the method 

used for adjusting for filtered air (FA) exposures in the data used to fit the MSS model does not 

use the subject-specific adjustments that are typically used in these clinical studies (ISA, p.6-4, 

6-5). Rather, the mean FA response across a study is used to adjust the O3 responses of each 

subject in the study (McDonnell et al., 2012, page 621). This adds additional uncertainty to the 

estimate of Var(U). 

The estimate of Var(U) in the MSS threshold model is 0.9373 (standard deviation 

0.9681). Since the actual values of U are bounded, we truncate the distribution of U at ±2 

standard deviations (±1.93), a convention we use for the distributions of several physiological 

variables input to APEX in the physiology input file. The results of sensitivity analyses of the 

MSS model predictions to the estimate of Var(U) are given in Table 6-15. Comparing the base 

case simulation to the simulation without any limits on U, we find that the results are not very 

sensitive to truncation of the distribution of U. Increasing or decreasing the value of the standard 

deviation of U, σ(U), does change the risk results significantly. As expected, the extreme case of 

setting all values of U to zero results in large changes in risk. 

Table 6-15. Sensitivity Analysis of the Inter-individual Variability Term U using the MSS 

Threshold Model. Percents of the population aged 5 to 18 with one or more and 6 or more 

days during the O3 season with lung function (FEV1) decrements more than 10, 15, and 

20% (Atlanta 2006 base case, ambient monitor data). 

Description 

st. dev. (U), ± limits on U 

1 or 

more 

∆FEV1

>10%

1 or 

more 

∆FEV1

>15%

1 or 

more 

∆FEV1

>20%

6 or 

more 

∆FEV1

>10%

6 or 

more 

∆FEV1

>15% 

6 or 

more 

∆FEV1

>20%

base: σ(U) = 0.9681, ± 1.93 31.77% 12.66% 6.55% 9.55% 3.08% 1.22%

σ(U) -50%= 0.4840, ± 0.9680 27.22% 4.85% 0.82% 3.64% 0.21% 0.01%

σ(U) +50%= 1.4522, ± 2.9044 35.53% 20.05% 13.70% 15.67% 8.31% 5.20%

σ(U)=0.9681, no limits on U 32.53% 14.18% 7.97% 10.86% 4.24% 2.20%

σ(U) = 0 (all U = 0) 25.26% 0.94% 0.00% 0.84% 0.00% 0.00%
6-43 

The MSS model estimated intra-individual variability Var(ε) has two basic components: 

(1) the intra-individual variability of the true response to O3 (both within-day and between-day) 

and (2) measurement error. These cannot be distinguished based on the available data. We are 

assuming that all of this variability is due to the true response, which will (absent other 

uncertainties) tend to overestimate the response to O3. We have conducted sensitivity analyses 

setting all ε to zero and also reducing the standard deviation of ε by 50%. These results of these 

are given in Table 6-16. Setting all ε to zero reduces the percent of children ages 5 to 18 with one 

or more FEV1 decrements ≥ 10% from 32% to 18%, for the scenario modeled (Atlanta, 2006 O3

season). Reducing the standard deviation of ε by 50% reduces these percents from 32% to 20%. 

The assumption of no measurement error in Var(ε) has the potential to significantly affect the 

risk results. 

The intra-individual variability term ε in equation 6-3 is assumed by the MSS threshold 

model to have a Gaussian distribution with mean zero and estimated standard deviation 4.135. 

As done for U, we truncate this variability term distribution at ±2 standard deviations (±8.27). To 

look at the effect of truncating the intra-individual variability distribution, we conducted 

simulations using the threshold model with this constraint relaxed. When fitting the MSS 

threshold model, the actual values of the intra-individual variability term range from about –20 

to 30 (McDonnell et al., 2012, Figure 3A). Truncating the distribution of ε at ±12, 16, and 20 

gives the results in Table 6-16, for ages 18 to 35. 

We see that this constraint has a very large effect on the results for percents of the 

population with FEV1 decrements ≥ 10 and 15% and less of an effect for 20%. The percent of 

children with one or more FEV1 decrements ≥ 10% increases from 31% to 92% when increasing 

the truncation point from 8.27 to 20. The estimates of six or more FEV1 decrements ≥ 10% are 

more stable, and therefore more reliable, increasing from 10% to 18% when increasing the 

truncation point from 8.27 to 20. Note that if the truncation limit is > 10, then there would be a 

nonzero probability of response >10% ΔFEV1 at zero O3 concentration (which would not be 

inconsistent with the observed clinical data). 

 Clearly the intra-individual variability Var(ε) in the MSS model is a key parameter and is 

influential in predicting the proportions of the population with FEV1 decrements > 10 and 15%. 

The assumption that the distribution of this term is Gaussian is convenient for fitting the model, 

but is not accurate. The extent to which this mis-specification affects the estimates of the 

parameters of the MSS model and its predictions is not clear. 
6-44 

Table 6-16. Sensitivity Analysis of the Intra-individual Variability Term ε using the MSS 

Threshold Model. Percents of the population aged 5 to 18 with one or more and 6 or more 

days during the O3 season with lung function (FEV1) decrements more than 10, 15, and 

20% (Atlanta 2006 base case, monitors air quality). 

Description 

1 or 

more 

∆FEV1

>10%

1 or 

more 

∆FEV1

>15%

1 or 

more 

∆FEV1

>20%

6 or 

more 

∆FEV1

>10%

6 or 

more 

∆FEV1

>15% 

6 or 

more 

∆FEV1

>20%

Base case, σ(ε) = 4.135 

Truncation of ε at ±8.27 31.77% 12.66% 6.55% 9.55% 3.08% 1.22%

Truncation of ε at ±12 91.71% 15.16% 7.15% 18.19% 3.41% 1.29%

Truncation of ε at ±16 91.71% 19.00% 7.21% 18.19% 3.44% 1.29%

Truncation of ε at ±20 91.71% 19.00% 7.23% 18.19% 3.44% 1.29%

σ(ε) = 0 (all ε = 0) 17.72% 9.38% 5.21% 6.07% 2.41% 1.01%

σ(ε) − 50% = 2.0665 

Truncation of ε at ±4.133 20.11% 10.04% 5.50% 6.63% 2.60% 1.06%

 McDonnell et al. (2013) have introduced another version of their model which assumes 

that Var(ε) increases with median response. So, with a fixed ventilation rate, Var(ε) will be larger 

for higher exposure concentrations and smaller for lower exposure concentrations. Simulations 

using their preferred model (Model 3) yield risk results higher than results based on the threshold 

model used for this HREA; those results are not presented here. 

6.5.2 Convergence of APEX Results 

APEX accounts for several sources of variability by drawing random variables from 

specified distributions. Some variables are drawn once for each simulated individual (e.g., age, 

location of residence), some are drawn every day or every hour for each simulated individual, 

and others are drawn more frequently, at the event level (e.g., activity). Increasing the number of 

individuals simulated in an APEX run increases the accuracy of the modeled variability and the 

results of the APEX runs are more reproducible. In order to assess the number of individuals to 

simulate to achieve convergence of APEX results, we perform multiple APEX runs with 

identical inputs except for the random number seed, and look at the variability of the results of 

these model runs. Table 6-17 summarizes the results of 40 APEX simulations of the Atlanta 

2006 base case with 200,000 simulated individuals. For each of these measures, the range of 

results over the 40 APEX runs is less than one percent. This analysis of the convergence of 

APEX results shows that modeling 200,000 simulated individuals is adequate for reasonable 

convergence of the FEV1 risk measures. 
6-45 

Table 6-17. Convergence results for the Atlanta 2006 base case with 200,000 simulated 

individuals. Percents of the population by age group with one or more days (and six or 

more days) during the O3 season with lung function (FEV1) decrements more than 10, 15, 

and 20%. Minimum and maximum values and ranges over 40 APEX runs. 

∆FEV1 ≥ 10% ∆FEV1 ≥ 15% ∆FEV1 ≥ 20% 

Age group Min Max Range Min Max range Min Max range

1 or more days in the season

5 to 18 31.3% 32.1% 0.88% 12.4% 12.9% 0.49% 6.21% 6.71% 0.50%

19 to 35 11.1% 11.5% 0.39% 3.00% 3.26% 0.26% 1.11% 1.32% 0.22%

36 to 55 3.54% 3.79% 0.25% 0.55% 0.68% 0.13% 0.13% 0.20% 0.07%

6 or more days in the season 

5 to 18 9.28% 9.73% 0.45% 2.80% 3.18% 0.38% 1.11% 1.37% 0.27%

19 to 35 1.09% 1.25% 0.16% 0.15% 0.21% 0.06% 0.03% 0.06% 0.03%

36 to 55 0.22% 0.30% 0.08% 0.01% 0.03% 0.02% 0.00% 0.01% 0.01%

6.5.3 Application of Model for All Lifestages 

The E-R functions derived from controlled human exposure studies involving 18-35 year 

old subjects were used to estimate responses for school-aged children (ages 5-18). This was in 

part justified by the findings of McDonnell et al. (1985) who reported that children 8-11 years 

old experienced FEV1 responses similar to those observed in adults 18-35 years old when both 

groups were exposed to 120 ppb O3 at an EVR of 32-35 L/min/m2

. In addition, a number of 

summer camp studies of school-aged children exposed in outdoor environments in the Northeast 

also showed O3-induced lung function changes similar in magnitude to those observed in 

controlled human exposure studies using adults, although the studies may not directly 

comparable. The MSS model predicts increasing responsiveness with younger participants in the 

age range of 18-35 years, as shown in Figure 6E-4 (Appendix 6E), which might indicate that 

responsiveness would continue to increase as age decreases from 18. In extending the MSS 

model to children, we fixed the age term in the model at its highest value, the value for age 18. If 

continuing the MSS model trend were to accurately describe continued increased response in 

children, then the fixed age term for children may have underestimated the effects on children, 

and particularly younger children. On the other hand, if FEV1 responses for children are similar 

to those observed in adults 18-35 years old, as the evidence suggests, then our approach to 

extending the age term (using the most responsive age of the range of 18-35) would overestimate 

the response to children (see Table 6E-3 in Appendix 6E). 
6-46 

In considering extending the MSS model to ages older than 36, we note that, in general, 

O3 responsiveness steadily declines for people aged 35-55, with people >55 eliciting minimal 

responsiveness (ISA, section 6.2.1.1). As described in Section 6.2.4, we extended the age term 

from the value at 36 linearly to zero at age 55, and set it to zero for ages above 55 (see Table 

6-2). The uncertainty of this extrapolation may be substantial, but these age groups are not the 

primary focus in the clinical risk assessment. 

6.5.4 Application of Model for Asthmatic Children 

The risk assessment used the same E-R relationship, developed from data collected from 

healthy study subjects, and applied it to all people, children, and asthmatic children. Based on 

limited evidence from a few human exposure studies, it is likely that subjects having asthma are 

at least as sensitive to acute effects of O3 as other subjects not having this health condition (ISA, 

page 6-20 to 6-21). An analysis by Romieu et al. (2002) indicated a larger O3-associated 

decrement in FEV1 among children with moderate to severe asthma than among all children with 

asthma (ISA, page 6-54). This suggests that the lung function decrements presented in this 

assessment for asthmatic children may be underestimated. The magnitude of influence this 

element might have on our risk estimates remains unknown at this time. In addition, asthmatic 

children may have less reserve lung capacity to draw upon when faced with decrements, and 

therefore a ≥10% decrement in lung function may be a more adverse event in an asthmatic child 

than a healthy child. 

6.5.5 Interaction Between Ozone and Other Pollutants 

Because the controlled human exposure studies used in the risk assessment involved only 

O3 exposures, it was assumed that estimates of O3-induced health responses would not be 

affected by the presence of other pollutants (e.g., SO2, PM2.5, etc). The magnitude of influence 

that potential interactions might have on our risk estimates remains unknown at this time. 

6.5.6 2000 vs. 2010 Population Demographics 

The population demographics used in the exposure modeling are based on the 2000 

Census. These are tract-level counts of population by age and sex, tract-level employment 

probabilities by age and sex, and tract-to-tract commuting patterns. We are modeling the years 

2006 to 2010, and some uncertainty will result from using demographics for a different year than 

being modeled. To assess the extent of this uncertainty, APEX runs were conducted for seven 

study areas using the 2010 Census and the results compared with APEX runs based on 2000 

Census data. Table 6-18 presents the percents of children (ages 5 to 18) with one or more FEV1

decrements ≥ 10, 15, 20%, for the 2010 modeling year, existing standard scenario, for APEX 

runs based on 2000 and 2010 Census data. Table 6-19 gives the relative changes of the results in 
6-47 

Table 6-18 from using 2000 demographics to using 2010 demographics. The largest relative 

changes occur in Cleveland and Detroit. For example, in Detroit, 1.845% of children have at 

least one ΔFEV1 ≥ 20% using 2000 Census data, while that number is 1.723% using 2010 

Census data. This is a relative reduction of 6.6 percent. 

Table 6-18. Comparison of 2000 vs. 2010 Census Demographics. Percents of all Schoolaged Children (ages 5 to 18) with One or More Days during the O3 Season with Lung 

Function (FEV1) Decrements more than 10, 15, and 20% (7 study areas, 2010 existing 

standard air quality). 

2000 Census Demographics 2010 Census Demographics 

Study Area ∆FEV1 ≥10% ∆FEV1 ≥15% ∆FEV1 ≥20% ∆FEV1 ≥10% ∆FEV1 ≥15% ∆FEV1 ≥20%

Atlanta 17.57% 4.55% 1.74% 17.08% 4.40% 1.67% 

Boston 14.32% 3.76% 1.40% 14.07% 3.67% 1.42% 

Cleveland 14.20% 3.43% 1.24% 13.79% 3.24% 1.17% 

Detroit 16.50% 4.62% 1.85% 15.93% 4.46% 1.72% 

Houston 16.34% 4.61% 1.83% 16.23% 4.54% 1.83% 

Los Angeles 16.01% 3.60% 1.20% 15.57% 3.49% 1.21% 

Sacramento 11.25% 2.44% 0.85% 11.22% 2.56% 0.83% 

Table 6-19. Comparison of 2000 vs. 2010 Census Demographics. Changes from using 2000 

Demographics to using 2010 Demographics of Percents of all School-aged children (ages 5 

to 18) with One or More Days during the O3 Season with Lung Function (FEV1) 

Decrements more than 10, 15, and 20% (7 study areas, 2010 existing standard air quality). 

Study Area ∆FEV1 ≥10% ∆FEV1 ≥15% ∆FEV1 ≥20% 

Atlanta (2.8%) (3.2%) (4.3%) 

Boston (1.8%) (2.6%) 1.4% 

Cleveland (2.9%) (5.5%) (5.9%) 

Detroit (3.5%) (3.6%) (6.6%) 

Houston (0.7%) (1.4%) 0.0% 

Los Angeles (2.8%) (3.1%) 0.4% 

Sacramento (0.3%) 5.1% (1.8%) 
6-48 

6.5.7 Qualitative Assessment of Uncertainty 

EPA staff have identified key sources of uncertainty with respect to the lung function risk 

estimates. These are: the physiological model in APEX for ventilation rates, the O3 exposures 

estimated by APEX, the MSS model applied to ages 18 to 35, and extrapolation of the MSS 

model to children ages 5 to 18. The first two of these are discussed in Chapter 5. At this time we 

do not have quantitative estimates of uncertainty for any of these. Table 6-20 provides a 

qualitative assessment of the uncertainty resulting from each of these key sources. The primary 

source of uncertainty is the MSS model, applied to ages 18 to 35. 
6-49 

Table 6-20. Summary of Qualitative Uncertainties of Key Modeling Elements in the O3 Lung Function Ri

Source Description 

Potential influence of 

uncertainty on risk 

estimates 

KnowledgeBase 

Direction Magnitude uncertainty* Com

The physiological model in APEX for ventilation rates 

The physiological model in APEX takes into account the population distribution of individual physiological characteristics and activities and models minute-by-minute ventilation rates for each simulated individual using a series of physiological relationships known with varying degrees of certainty. 

Over Low- Medium Low-Medium 

Ventilation rates are a key inFigure 6E-3 in Appendix 6E physiological model in APEX Comparisons with ventilation 

show fairly good agreement (Section 5.4.4). 

O3 exposures 

The O3 exposures estimated by APEX 

and their uncertainties are discussed in Chapter 5. 

Both Low- Medium Low O3 exposures are a key inpu

The McDonnellStewart-Smith (MSS) FEV1 model for ages 18 to 35 

The MSS model is integrated into APEX and predicts FEV1 decrements 

for each simulated individual. 

Both Medium- High Low 

There is a good conceptual f

this model, but the variability 

estimated parameters of the into the model predictions of 

estimated parameters have f(Table 6-14) and the risk resparameters (Figure 6-12). The most influential parametventilation rate is raised in thfive percent in β6 leads to a modeled number of children 

(The 95 percent confidence estimate is ±14%) We are unable to quantitativMSS model, since all of the and coworkers to fit the MSS EPA (in particular, some stud
6-50 

Source Description 

Potential influence of 

uncertainty on risk 

estimates 

KnowledgeBase 

Direction Magnitude uncertainty* Com

Inter-individual (between-individual) variability in the MSS FEV1 model 

Inter-individual variability (Var(U)) reflects the variability in responsiveness of individuals to O3. 

Both Medium Low 

In order to estimate Var(U), clinical trials using the same these in the data used to fit tdifficult to reliably estimate Vused for adjusting for filtered used to fit the MSS model doadjustments that are typically Rather, the mean FA responadjust the O3 responses of e

adds additional uncertainty tIf Var(U) is underestimated, number of people experienc

20% will be overestimated (auncertainty). This is because between-individual variability variability, so more responsivsee repeated occurrences of responsive individuals are mof high ∆FEV1. 

There are few clinical data folungs (i.e., asthma) and the for the increase in inter-indivreflect this or the increased vThis increase in inter-individoffset with a decrease in intrwould tend to increase the eat risk for large lung function element missing from the MS
6-51 

Source Description 

Potential influence of 

uncertainty on risk 

estimates 

KnowledgeBase 

Direction Magnitude uncertainty* Com

Intra-individual (withinindividual) variability in the MSS FEV1 model 

The intra-individual variability Var(ε) has two basic components: (1) the intra-individual variability of the true response to O3 (both within-day and 

between-day) and (2) measurement error. These cannot be distinguished based on the available data. We are assuming that all of this variability is due to the true response, which will (absent other uncertainties) tend to overestimate the response to O3. 

Over Medium- High Low 

The variability term ε is assu

a Gaussian distribution with standard deviation 4.135. Sibounded, we truncate the vastandard deviations (±8.27). truncating the variability distrsensitivity analyses with the different levels. We find that on estimates of percents of t

decrements ≥ 10 and 15% aThe percent of children with 

increases from 31% to 92% point from 8.27 to 20. The es

decrements ≥ 10% are more reliable, increasing from 10% truncation point from 8.27 to is too low, then (absent otheunderestimate the response 

Clearly the intra-individual vamodel is a key parameter anproportions of the population 

and 15%. The assumption thGaussian is convenient for fiaccurate. The extent to whicthe estimates of the parametpredictions is not clear. 

Extrapolation of the MSS model to children (ages 5 to 18) 

The MSS model is based on studies with subjects ranging in age from 18 to 35 years; therefore prediction for children involves assumptions for extrapolation of the MSS model for individuals <18 years of age. 

Both Medium Low 

Summer camp studies and oindicate that FEV1 responses 

those observed in adults 18-Section 6.5.3. 

* Refers to the degree of uncertainty associated with our understanding of the phenomenon, in the context of assessing and characterizi
6-52 

6.6 KEY OBSERVATIONS 

This lung function risk assessment evaluated risks of lung function decrements due to O3

exposure for three age study groups: school-aged children ages 5 to 18, young adults ages 19 to 

35, and adults ages 36 to 55. Lung function risks were estimated for 15 study areas: Atlanta, 

Baltimore, Boston, Chicago, Cleveland, Dallas, Denver, Detroit, Houston, Los Angeles, New 

York, Philadelphia, Sacramento, St. Louis, and Washington, DC. We estimated the percent of 

the study groups experiencing a reduction in lung function for three different levels of impact, 

10, 15, and 20% decrements in FEV1. These levels of impact were selected based on the 

literature discussing the adversity associated with these types of lung function decrements (U.S. 

EPA, 2012, Section 6.2.1.1; Henderson, 2006). 

 Individual versus Population-based Exposure-Response Model: Two models were 

used, one based on application of an individual level E-R function (the MSS model 

introduced in this review) and one based on application of a population level E-R 

function consistent with the model used in the previous O3 review which applies 

probabilistic population-level E-R relationships for lung function decrements (measured 

as percent reductions in FEV1) associated with 8-hr moderate exertion exposures. The 

MSS model is preferred, due to its ability to model individual exposures for a wide range 

of exposure times and levels of exercise as well as for exposures with time-varying 

exposures and levels of exercise (Section 6.2.4; ISA pages 6-15 to 6-16). The MSS model 

risk estimates are significantly higher than those estimated using the E-R approach. For 

lung function responses greater than 10, 15, and 20% the MSS model gives results 

typically a factor of three higher than the E-R model for school-aged children. Both 

models give higher responses for higher concentrations, compared to lower 

concentrations, as can be seen in Figures 6-6, 6-9, and 6-10. 

 Study Group Variability in Estimated Risk: When considering the study groups 

characterized by ages, school-aged children had the greatest percent of persons 

experiencing FEV1 decrements (e.g., Table 6-4). Adults >55 years old have minimal O3-

induced lung function risk considering any of the air quality scenarios. The MSS model 

was applied to estimate lung function risk for outdoor workers (ages 19-35) in Atlanta for 

one year (2006). The proportion of outdoor workers with FEV1 decrements ≥ 15% ranges 

from 3.6 to 5.3 times the proportion of the general population (ages 19-35) with FEV1

decrements ≥ 15% across the different standards simulated. The proportion of outdoor 

workers with multiple occurrences of FEV1 decrements ≥ 15% is much greater than for 

the general population. 
6-53 

 Year-to-Year Variability in Estimated Risk: Based on the MSS model, the percents of 

population estimated to experience lung function responses greater than 10, 15, and 20%, 

associated with O3 exposure while engaged in various levels of exertion, vary 

considerably for different years and study areas under the recent air quality scenarios and 

also for the existing and alternative standard scenarios (Figure 6-7 and Figure 6-8, Table 

6-4 and Table 6-5). For instance, the estimates for ≥ 10% FEV1 decrement for all schoolaged children for recent O3 concentrations range across study areas and years from 11 to 

31 percent, and range from 11 to 22 percent after simulating just meeting the existing 

standard. The estimates for ≥ 15% FEV1 decrement for all school-aged children for recent 

O3 concentrations range across study areas and years from 2 to 12 percent, and range 

from 2 to 6 percent after simulating just meeting the existing standards. The estimates for 

≥ 20% FEV1 decrement for recent O3 concentrations range across study areas and years 

from 1 to 6 percent, and range from 1 to 3 percent after simulating just meeting the 

existing standards. 

 Impact of Alternative Air Quality Scenarios: Figure 6-13 displays the risks and the 

incremental increases in risk for increasing standard levels, where risk is taken to be the 

highest value for each study area (over years) of the percent of school-aged children with 

FEV1 decrement ≥ 10%. The risks in this figure for Washington, DC, for example, are 

about 9.6% for the alternative standard level of 60 ppb and 13.4% for the alternative 

standard level of 65 ppb. The length of the orange bar is the incremental risk (3.8%) in 

going from the 60 ppb to the 65 ppb alternative standards. This figure shows that there 

are significant increases in incremental risk for all 15 study areas in the progression of 

alternative standard levels from 60 ppb to the level of the existing standard, 75 ppb. The 

pattern of reductions for lung function decrements larger than 15 and 20% are similar. As 

discussed in Section 4.3.1, the New York 60 ppb alternative standard was not modeled 

and the risk for NY for that scenario would not necessarily be zero. Figure 6-14 displays 

the risks and the incremental increases in risk for increasing standard levels, where risk is 

taken to be the mean value for each study area (over years) of the percent of school-aged 

children with FEV1 decrement ≥ 10%. 
6-54 

Figure 6-13. Lung Function Risk Results, Incremental Increases In Risk For Increasing Standard Levels: School-aged Children With FEV1 Decrement ≥ 10%, Highest Value For Each Study area Over Years66 New York level 60 was not modeled. We do not know what the percent risk would be for NY under the 60 ppb alternative standard, b

be zero. 

standard level (ppb) 60 65 70 75

WashingtonSt LouisSacramentoPhiladelphiaNew YorkLos AngelesHoustonDetroitDenverDallasClevelandChicagoBostonBaltimoreAtlanta

percent of school-aged children with FEV1 decrement > 10%

0% 2% 4% 6% 8% 10% 12% 14% 16% 18% 20% 22
6-55 

Figure 6-14. Lung Function Risk Results, Incremental Increases In Risk For Increasing Standard Levels: School-aged Children With FEV1 Decrement ≥ 10%, Mean Value For Each Study Area Over Years7

7 New York level 60 was not modeled. We do not know what the percent risk would be for NY under the 60 ppb alternative standard, b

be zero. 

standard level (ppb) 60 65 70 75

WashingtonSt LouisSacramentoPhiladelphiaNew YorkLos AngelesHoustonDetroitDenverDallasClevelandChicagoBostonBaltimoreAtlanta

percent of school-aged children with FEV1 decrement > 10%

0% 2% 4% 6% 8% 10% 12% 14% 16% 18% 
6-56 

6.7 REFERENCES 

Adams, W.C. 2002. Comparison of chamber and face-mask 6.6-hour exposures to ozone on 

pulmonary function and symptoms responses. Inhalation Toxicology. 14:745-764. 

Adams, W.C. 2003. Comparison of chamber and face mask 6.6-hour exposure to 0.08 ppm 

ozone via square-wave and triangular profiles on pulmonary responses. Inhalation 

Toxicology. 15:265-281. 

Adams, W.C. 2006. Comparison of chamber 6.6-h exposures to 0.04-0.08 ppm ozone via squarewave and triangular profiles on pulmonary responses. Inhalation Toxicology. 18:127-136. 

American Thoracic Society. 2000. What constitutes an adverse effect of air pollution?. American 

Journal of Respiratory and Critical Care Medicine. 161:665-673. 

Bittar, E. Edward, editor. 2002. Pulmonary Biology in Health and Disease. Springer, New York. 

Box, G.E.P. and G.C. Tiao. 1973. Bayesian Inference in Statistical Analysis. Wesley Publishing 

Co.: Wiley Classic Library, ISBN 0-471-57428-7. 

Burmaster, D.E. 1998. Lognormal distributions for skin area as a function of body weight. Risk 

Analysis. 18(1):27-32. 

Dietert, R.R.; R.A. Etzel; D. Chen, et al. 2000. Workshop to identify critical windows of 

exposure for children’s health: immune and respiratory systems work group summary." 

Environ Health Perspect. 108(S3):483-490. 

Esmail, S.; Y. Bhambhani and S. Brintnell. 1995. Gender differences in work performance on the 

Baltimore therapeutic equipment work simulator. American Journal of Occupational 

Therapy. 49:405 - 411. 

Federal Register. 1996. Responses to Significant Comments on the 1996 Proposed Rule on the 

National Ambient Air Quality Standards for Ozone (December 13, 1996; Fed. Reg. 61 

FR 65716). 

Folinsbee, L.J., et al. 1988. Pulmonary function and symptom responses after 6.6-hour exposure 

to 0.12 ppm ozone with moderate exercise. Journal of the Air Pollution Control 

Association. 38:28-35. 

Graham, S.E. and T. McCurdy. 2005. Revised Ventilation Rate (VE) Equations for Use in 

Inhalation-oriented Exposure Models. Washington, DC: EPA Office of Air and 

Radiation. (EPA document number EPA/600/X-05/008, Appendix A). 

<http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=202543>. 

Hazucha, M.J.; L.J. Folinsbee and P.A. Bromberg. 2003. Distribution and reproducibility of 

spirometric response to ozone by gender and age. Journal of Applied Physiology. 

95(5)1917-1925. 

Hislop, A.A. 2002. Airway and blood vessel interaction during lung development. Journal of 

Anatomy. 201:325–334. Available at: 

<www.ncbi.nlm.nih.gov/pmc/articles/PMC1570917/>. 

Horstman, D.H. et al. 1990. Ozone concentration and pulmonary response relationships for 6.6-

hour exposures with five hours of moderate exercise to 0.08, 0.10, and 0.12 ppm. 

American Review of Respiratory Disease. 142:1158-1163. 
6-57 

Isaacs, K.; G. Glen; T. McCurdy and L. Smith. 2008. Modeling energy expenditure and oxygen 

consumption in human exposure models: accounting for fatigue and EPOC. Journal of 

Exposure Science and Environmental Epidemiology. 18:289–298. 

Isaacs, K. and L. Smith. 2005. New Values for Physiological Parameters for the Exposure Model 

Input File Physiology, text memorandum submitted to the U.S. Environmental Protection 

Agency under EPA Contract EP-D-05-065. NERL WA 10. Alion Science and 

Technology. Found in US EPA. (2009). Risk and Exposure Assessment to Support the 

Review of the SO2 Primary National Ambient Air Quality Standard. (EPA document 

number EPA-452/R-09-007, August 2009). 

<http://www.epa.gov/ttn/naaqs/standards/so2/data/200908SO2REAFinalReport.pdf>. 

Kim, C.S.; N.E. Alexis; A.G. Rappold; H. Kehrl; M.J. Hazucha; J.C. Lay; M.T. Schmitt; M. 

Case; R.B. Devlin; D.B. Peden; D. Diaz-Sanchez. 2011. Lung function and inflammatory 

responses in healthy young adults exposed to 0.06 ppm ozone for 6.6 hours. American 

Journal of Respiratory and Critical Care Medicine. 183:1215-1221. 

Linn, W.S.; R.D. Buckley; C.E. Spier; R.L. Blessey; M.P. Jones; D.A. Fischer and J.D. Hackney. 

1978. Health effects of ozone exposure in asthmatics. The American Review of 

Respiratory Disease. 117(5)835-843. 

Lunn, D.; C. Jackson; N. Best; A. Thomas and D. Spiegelhalter. 2012. The BUGS Book - A 

Practical Introduction to Bayesian Analysis. CRC Press: Chapman and Hall. 

McCurdy, T.; G. Glen; L. Smith; Y. Lakkadi. 2000. The National Exposure Research 

Laboratory's Consolidated Human Activity Database. Journal of Exposure Analysis and 

Environmental Epidemiology. 10:566-578. 

McDonnell, W.F.; R.S. Chapman; M.W. Leigh; G.L. Strope; A.M. Collier. 1985. Respiratory 

responses of vigorously exercising children to 0.12 ppm ozone exposure. American 

Review of Respiratory Disease. 132:875-879. 

McDonnell, W.F.; H.R. Kehrl; S. Abdul-Salaam; P.J. Ives; L.J. Folinsbee; R.B. Devlin; J.J. 

O’Neil; D.H. Horstman. 1991. Respiratory response of humans exposed to low levels of 

ozone for 6.6 hours. Archives of Environmental Health. 46(3):145-150. 

McDonnell, W.F. et al. 1993. Predictors of individual differences in acute response to ozone 

exposure. American Review of Respiratory Disease. 147:818-825. 

McDonnell, W.F. et al. 1997. Prediction of ozone-induced FEV1 changes. American Journal of 

Respiratory and Critical Care Medicine. 156:715-722. 

McDonnell, W.F.; P.W. Stewart and M.V. Smith. 2007. The temporal dynamics of ozoneinduced FEV1 changes in humans: an exposure-response model. Inhalation Toxicology. 

19:483-494. 

McDonnell, W.F.; P.W. Stewart and M.V. Smith. 2010. Prediction of ozone-induced lung 

function responses in humans. Inhalation Toxicology. 22(2):160-8. 

McDonnell, W.F.; P.W. Stewart; M.V. Smith; C.S. Kim and E.S. Schelegle. 2012. Prediction of 

lung function response for populations exposed to a wide range of ozone conditions. 

Inhalation Toxicology. 24:619-633. 
6-58 

McDonnell, W.F.; P.W. Stewart and M.V. Smith. 2013. Ozone exposure-response model for 

lung function changes: an alternate variability structure. Inhalation Toxicology. 25:348-

353. 

Narayanan, M.; J. Owers-Bradley; C.S. Beardsmore; M. Mada; I. Ball; R. Garipov; K.S. Panesar; 

C.E. Kuehni; B.D. Spycher; S E. Williams; M. Silverman. 2012. Alveolarization 

continues during childhood and adolescence: new evidence from helium-3 magnetic 

resonance." American Journal of Respiratory and Critical Care Medicine. 185(2):86-

191. Available at: <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3410735/>. 

Passannante, A.N.; M.J. Hazucha; P.A. Bromberg; E. Seal; L. Folinsbee; G. Koch. 1998. 

Nociceptive mechanisms modulate ozone-induced human lung function decrements. 

Journal of Applied Physiology. 85:1863-1870. 

Romieu, I; J.J. Sienra-Monge; M. Ramirez-Aguilar; M.M. Tellez-Rojo; H. Moreno-Macias; N.I. 

Reyes-Ruiz; B.E. Del Rio-Navarro; M.X. Ruiz-Navarro; G. Hatch; R. Slade; M. 

Hernandez-Avila. 2002. Antioxidant supplementation and lung functions among children 

with asthma exposed to high levels of air pollutants. American Journal of Respiratory 

and Critical Care Medicine. 166:703-709. 

Samet, J.M. 2011. Clean Air Scientific Advisory Committee (CASAC) Response to Charge 

Questions on the Reconsideration of the 2008 Ozone National Ambient Air Quality 

Standards. (Report number EPA-CASAC-11-004), dated March 30, 2011. Available at: 

<http://yosemite.epa.gov/sab/sabproduct.nsf/0/F08BEB48C1139E2A8525785E006909A

C/$File/EPA-CASAC-11-004-unsigned+.pdf>. 

Schelegle, E.S.; C.A. Morales; W.F. Walby; S. Marion; R.P. Allen. 2009. 6.6-hour inhalation of 

ozone concentrations from 60 to 87 ppb in healthy humans. American Journal of 

Respiratory and Critical Care Medicine. 180:265-272. 

Schelegle, E.S.; W.C. Adams; W.F. Walby and S. Marion. (2012). Modeling of individual 

subject ozone exposure response kinetics. Inhalation Toxicology. 24(7):401-415. 

Schofield, W.N. 1985. Predicting basal metabolic rate, new standards and review of previous 

work. Clinical Nutrition. 39C(suppl):5-41. 

Seal, Jr., E.; W.F. McDonnell; D.E. House. 1996. Effects of age, socioeconomic status, and 

menstrual cycle on pulmonary response to ozone. Archives of Environmental and 

Occupational Health. 51:132-137. 

U.S. EPA. 1996. Review of National Ambient Air Quality Standards for Ozone: Assessment of 

Scientific and Technical Information - OAQPS Staff Paper. Research Triangle Park, NC: 

EPA Office of Air Quality Planning and Standards. (EPA document number EPA/452/R96-007). Available at: <http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_pr.html>. 

U.S. EPA. 2007a. Review of National Ambient Air Quality Standards for Ozone: Policy 

Assessment of Scientific and Technical Information - OAQPS Staff Paper. Research 

Triangle Park, NC: EPA Office of Air Quality Planning and Standards. (EPA document 

number EPA-452/R-07-007). Available at: 

<http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_sp.html>. 
6-59 

U.S. EPA. 2007b. Ozone Population Health Risk Assessment for Selected Urban Areas. 

Research Triangle Park, NC: EPA Office of Air Quality Planning and Standards. (EPA 

document number EPA-452/R-07-009). Available at: 

<http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html>. 

U.S. EPA. 2009. Metabolically Derived Human Ventilation Rates: A Revised Approach Based 

Upon Oxygen Consumption Rates. Washington, DC: EPA National Center for 

Environmental Assessment. (EPA document number EPA/600/R-06/129F). Available at: 

<http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=202543>. 

U.S. EPA. 2011. O3 National Ambient Air Quality Standards: Scope and Methods Plan for 

Health Risk and Exposure Assessment. Research Triangle Park, NC: EPA Office of Air 

Quality Planning and Standards. (EPA document number EPA-452/P-11-001). Available at: 

<http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_2008_pd.html>. 

U.S. EPA. 2012a. Total Risk Integrated Methodology (TRIM) - Air Pollutants Exposure Model 

Documentation (TRIM.Expo / APEX, Version 4.4) Volume I: User’s Guide. Research 

Triangle Park, NC: EPA Office of Air Quality Planning and Standards. (EPA document 

number EPA-452/B-12-001a). Available at: 

<http://www.epa.gov/ttn/fera/human_apex.html>. 

U.S. EPA. 2012b. Total Risk Integrated Methodology (TRIM) - Air Pollutants Exposure Model 

Documentation (TRIM.Expo / APEX, Version 4.4) Volume II: Technical Support Document. 

Research Triangle Park, NC. (EPA document number EPA-452/B-12-001b). Available at: 

<http://www.epa.gov/ttn/fera/human_apex.html>.

U.S. EPA. 2013. Integrated Science Assessment of Ozone and Related Photochemical Oxidants. 

EPA National Center for Environmental Assessment. (EPA document number EPA/600/R10/076F, 2013). Available at: 

<http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_2008_isa.html >. 

WinBUGS, version 1.4.3. Available at: 

<http://www.mrc-bsu.cam.ac.uk/bugs/winbugs/contents.shtml>. 

 
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7-1 

7 CHARACTERIZATION OF HEALTH RISK BASED ON 

EPIDEMIOLOGICAL STUDIES 

This chapter provides an overview of the methods used to estimate health risks in 

selected urban areas based on application of results of epidemiology studies. Section 7.1.1 

discusses the basic structure of the risk assessment, identifying the modeling elements and 

related sources of input data needed for the analysis and presenting an overview of the approach 

used in calculating health effect incidence using concentration-response (C-R) functions based 

on epidemiological studies. Section 7.2 discusses air quality considerations. Section 7.3 

discusses the selection of model inputs including: (a) selection of urban study areas, (b) selection 

of epidemiological studies and specification of C-R functions, (c) specification of baseline health 

effect incidence and prevalence rates, and (d) estimation of population (demographic) counts. 

Section 7.4 describes how uncertainty and variability are addressed in the risk assessment, 

including specification of the sensitivity analyses completed for the risk assessment and how 

these differ from the core risk estimates. Section 7.5 summarizes the risk estimates that are 

generated, including both the core estimates and sensitivity analyses. Finally, Section 7.6 

provides an assessment of overall confidence in the risk assessment together with a set of key 

observations regarding the risk estimates generated. 

7.1 GENERAL APPROACH 

7.1.1 Basic Structure of the Risk Assessment 

This risk assessment involves the estimation of the incidence of specific health effect 

endpoints associated with exposure to ambient O3 for defined populations located within a set of 

urban study areas. Because the risk assessment focuses on health effect incidence experienced by 

defined populations, it represents a form of population-level risk assessment and does not 

estimate risks to individuals within the population. Furthermore, because it models risk for 

populations within a set of selected urban study areas, it is not intended to provide an estimate of 

national-scale risk.1

 

 The general approach used in this component of the O3 risk assessment relies on C-R 

functions based on effect estimates and model specifications obtained from epidemiological 

studies. Because these studies derive effect estimates and model specifications using averages of 

ambient air quality data from fixed-site, population-oriented monitors, uncertainty arising from 

the application of these functions in an O3 risk assessment is decreased if, in modeling risk, we 

 

1

 Chapter 8 provides a limited assessment of national risk focused on the mortality burden associated with 2007 

ambient O3 concentrations. 
7-2 

also use ambient air quality data at fixed-site, population-oriented monitors to characterize 

exposure. Therefore, we developed a composite monitor for each urban study area to represent a 

surrogate population exposure by averaging O3 concentrations across the monitors in that study 

area to produce a single composite hourly time-series of values. The O3 metrics used in 

evaluating risk are derived from the composite monitor hourly time-series distribution (see 

sections 7.2 and Chapter 4 for additional detail on the characterization of ambient O3 levels).2

The general O3 health risk model used here, illustrated in Figure 7-1, combines O3 air 

quality data, C-R functions, baseline health incidence and prevalence data, and population data 

(all specific to a given urban study area) to derive estimates of the annual incidence of specified 

health effects for that urban study area attributable to O3 exposure. Twelve urban study areas 

were selected to provide coverage for the types of urban O3 scenarios likely to exist across the 

U.S. (see section 7.3.1). Chapter 8 provides an assessment of the degree to which risk-related 

attributes in the 12 selected urban areas are representative of other urban areas in the U.S. 

This assessment estimates health risk associated with recent ambient O3 conditions and 

for air quality adjusted to just meet the existing 8-hour (8-hr) O3 standard, and additional 

estimates of risk if alternative standards are just met, with an emphasis on reductions in risk 

between just meeting the existing standard and just meeting alternative standards (the full set of 

risk estimates, including simulation of risk under current conditions is presented in Appendix 

7B). The alternative standard levels evaluated are 70, 65 and 60 ppb (expressed using the 

existing form and averaging time of the O3 standard). 

We simulated just meeting the existing and alternative O3 standards by adjusting hourly 

O3 concentrations measured over the O3 season using a model-based adjustment methodology 

that estimates O3 sensitivities to precursor emissions changes.3 These sensitivities, which 

estimate the response of O3 concentrations to reductions in anthropogenic NOx and VOC 

emissions, are developed using the Higher-order Decoupled Direct Method (HDDM) capabilities 

in the Community Multi-scale Air Quality (CMAQ) model. More details on the HDDMadjustment approach is presented in Chapter 4 of this Health Risk and Exposure Assessment 

(HREA) and in Simon et al. (2013). 

As discussed in Chapters 2 and 3, in modeling risk we employ continuous non-threshold 

C-R functions relating O3 exposure to health effect incidence. The use of non-threshold functions 

 

2

 This holds for all air quality metrics used in modeling short-term mortality and morbidity endpoints. However, the 

air metric used in modeling long-term mortality is based on a seasonal mean of maximum hourly values derived 

for each O3 monitor within an urban study area with those individual averages then combined to generate a single 

seasonal average composite monitor value for each study area (see section 7.2 for more detail). 3

 In the first draft of this HREA, we used a statistical quadratic rollback approach to simulate just meeting the 

existing O3 standards. In that first draft, we proposed using the model based approach used in the current 

document, and received support for the model based approach from CASAC (Frey and Samet, 2012). 
7-3 

reflects the discussion of the relevant studies in the O3 ISA (U.S. EPA 2013a, section 2.5.4.4). 

However, also consistent with the conclusions of the O3 ISA, we recognize that the evidence 

from the studies indicates less confidence in specifying the shape of the C-R function at O3

concentrations towards the lower end of the distribution of data used in fitting the curve due to 

the reduction in the number of data points available. The O3 ISA noted that the studies indicate 

reduced certainty in specifying the shape of the C-R function specifically for short-term O3-

attributable respiratory morbidity and mortality, in the range generally below 20 ppb (for both 8-

hr maximum and 24-hr metrics) (O3 ISA, section 2.5.4.4). However, care needs to be taken in 

interpreting this range of reduced confidence indicated in the studies and applying it to the 

interpretation of risk estimates generated for a specific urban study area. This is because there is 

considerable heterogeneity in the effect of O3 on mortality across urban study areas (O3 ISA, 

section 6.6.2.3). Additionally, it is likely that levels of confidence associated with C-R functions 

(including ranges of reduced confidence in specifying the function) also vary across urban study 

areas reflecting underlying differences in factors impacting the exposure-response relationship 

for O3, such as demographic differences and exposure measurement error. For these reasons, the 

≤20 ppb range discussed in the O3 ISA should be viewed as a more generalized range to be 

considered qualitatively or semi-quantitatively, along with many other factors, when 

interpreting the risk estimates rather than as a fixed, bright-line.4 

Based on comments we received from CASAC on the 1st draft HREA (Frey and Samet, 

2012), we are no longer including estimates of risk down to the lowest measured level (LML).5

Instead, through the use of heat map tables, we focus on providing estimates of total risk, and the 

distribution of risk over concentrations of O3.

6

 Coupled with information about what the studies 

indicate about the C-R function at lower O3 concentrations, this provides for a more complete 

understanding of confidence in estimated risk than simply truncating risk at the LML. 

In modeling risk for all health endpoints included in the analysis, for recent O3 conditions 

and just meeting the existing standard, we estimated total risk (down to zero). For meeting the 

 

4

 This range of reduced confidence in the shape of the C-R function is most appropriately applied to area-wide 

averages (i.e., composite monitor values) of the type often used in epidemiological studies rather than to the range 

of O3 associated with a particular monitor. This reflects the fact that the observations presented in the O3 ISA are 

themselves based on consideration for epidemiological studies which use composite monitor values. 5

 Based on their November 19, 2012 letter commenting on the 1st draft HREA, CASAC recommended against 

inclusion of risk estimates based on the LML in the core analysis due to the fact that there is little difference 

between these estimates and risk estimates based on total O3 exposure and that LML information is not available 

for many of the epidemiological studies used in the HREA (Frey and Samet, 2012). However, they recommended 

a more limited exploration of the LML and its implications for risk for one or more areas. In response, we have 

included coverage for LML as part of our discussion of the heat maps results presented in section 7.5.1. 6

 Heat map tables illustrate the distribution of estimated O3-related deaths across daily O3 levels for each urban study 

and allow a quick visual comparison of trends (in the distribution of total O3 risk as we as risk reductions) across 

ambient O3 ranges both within and across study areas (see section 7.5). 
7-4 

existing and alternative standards, we estimated both total risk as well as the difference in risk, 

representing the degree of risk reduction associated with just meeting the existing and alternative 

standard levels. When calculating risk differences, we focus on comparing total risk after just 

meeting each alternative standard with total risk after just meeting the existing standards. We 

also evaluate the incremental change in risk from meeting increasingly lower alternative standard 

levels. Risk results are presented in terms of absolute numbers and changes in the O3-attributable 

incidence of mortality and morbidity, and in terms of the percent of baseline mortality and 

morbidity attributable to O3. We also provide risks per 100,000 population (to normalize risks 

across urban areas with different size populations to facilitate comparisons). 

As with previous NAAQS risk assessments, for this analysis we have generated two 

categories of risk estimates, including a set of core (or primary) estimates and an additional set of 

sensitivity analyses. The core risk estimates utilize C-R functions based on epidemiological 

studies for which we have relatively greater overall confidence and which provide the best 

coverage for the broader O3 monitoring period (rather than focusing only on the summer season). 

Although it is not strictly possible to assign quantitative levels of confidence to these core risk 

estimates due to data limitations, they are generally based on inputs having higher overall levels 

of confidence relative to risk estimates that are generated using other C-R functions. Therefore, 

emphasis is placed on the core risk estimates in making observations regarding total risk and risk 

reductions associated with recent conditions and after just meeting the existing and alternative 

standard levels. By contrast, the sensitivity analysis results typically reflect application of C-R 

functions covering a wider array of design elements which can impact risk (e.g., length of 

season, co-pollutants models, lag structures, statistical modeling methods etc). The sensitivity 

analysis results provide insights into the potential impact of these design elements on the core 

risk estimates, thereby informing our characterization of overall confidence in the core risk 

estimates.7

 We have significantly expanded our sensitivity analysis relative to that completed for 

earlier drafts of the HREA to address a wider range of modeling elements which can impact the 

core risk estimates. Details of the design of the core and sensitivity analyses (including modeling 

element composition) for each of the health effect endpoints categories covered in this risk 

assessment are presented in section 7.4.3 and briefly summarized below. 

 

7

 In presenting both the core and sensitivity analysis, we include both point estimates and 95th percentile confidence 

intervals (CIs). The 95th percentile CIs reflect the statistical fit of the underlying effect estimates and therefore 

reflect the statistical power of the epidemiological studies supplying the effect estimates. Often in comparing 

sensitivity analysis with core risk estimates, we focus not only on the point estimates, but also on the confidence 

intervals since these inform our understanding of confidence in the respective risk estimates. 
7-5 

For short-term exposure related mortality, our core analysis is based on application of CR functions obtained from the Smith et al. (2009) epidemiological study (see section 7.3.2). In 

addition, we have completed an expanded array of sensitivity analyses which provide coverage 

for a number of modeling elements including: (a) time period reflected in risk modeling (summer 

season versus full monitoring period), (b) peak O3 metric (8-hr maximum versus 8-hr mean) (c) 

use of regional versus national-based Bayesian adjustment in deriving effect estimates,8 (d) use 

of single (O3-only) versus co-pollutant (O3 and PM10) models, 9 (e) application of alternative C-R 

functions based on Zanobetti and Schwartz (2008) (see section 7.3.2) and (f) size of the urban 

study area (CBSA versus smaller multi-county study area)10 (see sections 7.4.3 and 7.5.3 for 

additional detail on the sensitivity analyses completed). In addition to these sensitivity analyses, 

we have considered alternative methods for adjusting air quality to just meet the existing and 

alternative standards (NOx-only versus combination of VOC and NOx reductions). Additional 

sensitivity analyses exploring lag structure may also provide useful information, but are not 

possible due to the lack of availability of Bayes adjusted estimates for alternative lag structures. 

For short-term exposure morbidity, we have effect estimates covering a wide range of 

design elements including co-/single-pollutant models and lag structure. However, we were not 

in a position to differentiate between these alternative model forms in terms of overall 

confidence and have therefore included all of these estimates in the core analysis. This range of 

risk estimates can also be viewed as a sensitivity analysis where there is no clear “core” estimate 

and instead, the full range of risk estimates is considered to provide the best overall picture of 

risk for a specific endpoint (see section 7.3.2 and 7.4.3). 

 

8

 Short-term O3-attributable mortality in this analysis is modeled using Bayesian-adjusted effect estimates. This 

approach involves adjustment of each city’s effect estimate using a prior distribution reflecting the O3-mortality 

relationship seen across the broader set of cities considered in the epidemiological study. For the sensitivity 

analysis, we compare the use of a national prior distribution (the core approach) for the Bayesian adjustment with 

use of a regional prior. 9

 The co-pollutants model results are limited by the reduced number of days with co-pollutants sampling (either 1 in 

3 or 1 in 6) which makes it difficult to evaluate the statistical significance of these results in view of the large 

posterior standard deviations (Smith et al., 2009). This increased uncertainty associated with the estimates 

prevents these results from being treated as part of the core analysis. Never the less, they provide perspective on 

the potential magnitude of risk associated with co-pollutants modeling and as such make an important 

contribution as a sensitivity analysis for short-term O3-attributable mortality. 10 Core based statistical areas (CBSAs) are U.S. geographic areas defined by the Office of Management and Budget 

(OMB). They include an urban center of at least 10,000 people combined with adjacent urban and suburban areas 

that are socioeconomically tied to the urban center by commuting. CBSAs tend to be significantly larger than the 

study areas used in the epidemiological studies providing effect estimates. We have used risk estimates based on 

CBSAs in the core analysis in order to better represent the changes in risk that could be experienced in the broader 

urban areas and to avoid the introduction of known bias into the risk assessment. We have included risk estimates 

based on the smaller study areas from the original epidemiological studies as sensitivity analyses (see discussion 

later in this section for additional detail). 
7-6 

Our analysis also includes estimates of long-term exposure related respiratory mortality, 

including a core estimate based on a co-pollutant model11 (with PM2.5) together with sensitivity 

analyses exploring regional heterogeneity in the effect estimate and application of a nationallevel estimates focusing only on O3, analyses based on findings reported by Jerrett et al. (2009) 

(see section 7.5.3). We have also included a sensitivity analysis exploring the impact of potential 

thresholds in the C-R relationship on estimates of long-term exposure-related mortality that were 

evaluated in Jerrett et al. (2009). The approach used and added study author interpretation of the 

published model results are further described in Sasser (2014) and in section 7.3.2. 

We modeled all core risk estimates using study areas based on the core-based statistical 

area (CBSA) regardless of whether the epidemiological studies providing the effect estimates 

used the CBSA spatial definition or a different spatial study area definition. The decision to use 

CBSA-based study areas in all core simulations reflects our desire to better represent the changes 

in risk that could be experienced in the urban areas and avoid introducing substantial known bias 

into the risk estimates. As discussed in Chapter 4 (section 4.3.1.2), most nonattainment O3

monitors are not located in the center of the urban area, but instead are sited in the surrounding areas, 

reflecting the transport and atmospheric chemistry governing O3 formation. The monitors in the 

urban core areas are usually most affected by local sources of NOx and experience lower 

concentrations of O3 since the NO is titrating O3 in these areas. For these monitors, simulating just 

meeting the existing and alternative standard levels can result in an increase in low level or mean 

O3 concentrations, while areas further out from the urban core experience the expected reduction 

in the highest O3 levels. Had we focused risk estimates on the smaller urban core areas used in 

some of the epidemiological studies, we would not have fully captured the changes in risk 

estimated to be experienced by the broader urban area since we would have been focusing only 

on those areas experiencing net increases in O3 (when simulating just meeting the existing and 

alternative standard levels). By modeling risk for the core analysis using the more inclusive 

CBSA study areas, we insure that risk estimates will include consideration both for the relatively 

smaller core urban areas experiencing increases in O3 as well as the broader urban and suburban 

area experiencing risk reductions associated with reductions in the highest O3 concentrations. We 

will also insure that, to a greater extent, the analysis includes the county with the design value 

monitor in the assessment of risk (see section 7.2). 

There is a degree of uncertainty introduced through application of effect estimates to 

study areas (i.e., CBSAs) that do not match those used in the underlying epidemiological studies. 

 

11 The seasonal average metrics used in the long-term mortality estimate are not very sensitive to the reduced 

number of days with co-pollutant monitoring, and as such it is appropriate to use the co-pollutant model in 

generating the core risk estimates. 
7-7 

This uncertainty should be viewed within the context of the overall larger uncertainty associated 

with transferring effect estimates from the context of the epidemiological studies to the context 

of the risk assessment. The epidemiological studies used in modeling short-term exposure-related 

endpoints generate effect estimates based on day to day variation in O3 and health effects, using 

the area wide average O3 concentrations. Area wide O3 averaging masks the specific population 

distribution of O3 exposures which reflects the times and durations of exposures to O3 measured 

at individual monitors in an urban area. We apply those effect estimates to the air quality 

scenarios of just meeting existing and alternative standards, where we are shifting the entire 

distribution of daily O3 concentrations, and altering the relationships between O3 concentrations 

at different monitors, and thus likely altering the relationship between area wide average O3 and 

the population distribution of O3 exposures. By doing so, we introduce an additional source of 

exposure measurement error, which goes beyond the impact that measurement error has on the 

effect estimate, and introduces additional uncertainty into the estimates of risk associated with 

simulating meeting existing and alternative standards. 

Our decision to use the CBSA to define the spatial extent of each urban study area 

reflects the greater weight we place on minimizing biases relative to minimizing uncertainty, 

although we strive to minimize both where possible. The sensitivity analysis related to using 

epidemiological study-based spatial definitions for urban areas shows clearly that using the 

smaller urban areas biases downward the risk reductions across an urban area. Thus, to avoid this 

bias in risk estimates we accept a measure of increased uncertainty associated with the 

application of effect estimates to study areas that are larger than those used in some of the 

original epidemiological studies providing those effect estimates. 

Using the CBSA definitions of urban areas can partially address the bias caused by 

focusing only on urban core areas. However, it does not address this bias fully in some areas 

because of the unevenness in monitoring throughout urban areas. In some urban areas the 

monitors are more evenly distributed across the CBSA, while in other areas they are not. For 

example, in some urban areas, there is a high density of monitors in the urban core counties, with 

less density of monitors in surrounding counties also in the CBSA. Because we use a simple 

average (to match the averaging used in the epidemiology studies) of monitors across the CBSA, 

this means that O3 concentrations in areas where there are more monitors (e.g. in urban core 

counties) will get a higher weight in the average O3 concentrations relative to O3 concentrations 

in other parts of the CBSA. To the extent that the area with the higher density of monitors 

experiences increases in O3 while the remaining area experiences decreases in O3, the overall 

average O3 concentrations applied to populations in the entire CBSA will be weighted more 

towards O3 increases, which will attenuate the overall risk reduction that may be associated with 

meeting alternative O3 standards. We are not able to determine the magnitude of this remaining 
7-8 

bias; however, it is expected to be higher in locations with a high percentage of total CBSA 

monitors concentrated in urban core counties. 

The risk assessment reflects consideration for five years of recent air quality data from 

2006 through 2010, with these five years reflecting two three-year averaging periods that share a 

common overlapping year (i.e., 2006-2008 and 2008-2010 - see section 7.2). We selected these 

two averaging periods to provide coverage for a more recent time period with relatively elevated 

O3 levels (2006-2008) and recent time period with relatively lower O3 levels (2008-2010). For 

the HREA, we model risk for the middle year of each three-year averaging period in order to 

provide estimates of risk for a year with generally higher O3 levels (i.e., 2007) and a year with 

generally lower O3 levels (i.e., 2009). In modeling risk, we matched the population data used in 

the risk assessment to the year of the air quality data. For example, when we used 2007 air 

quality data, we used 2007 population estimates. For baseline incidence and prevalence, rather 

than interpolating rates for the two specific years modeled in the risk assessment, we selected the 

closest year for which we had existing incidence/prevalence data (i.e., for simulation year 2007, 

we used available data for 2005 and for simulation year 2009, we used data from 2010). The 

calculation of baseline incidence and prevalence rates is described in section 7.3.4. 

The risk assessment procedures described in more detail below are diagramed in Figure 

7-1. To estimate the change in incidence of a given health effect resulting from a given change in 

ambient O3 concentrations in an assessment location, the following analysis inputs are necessary: 

 Air quality information including: (1) O3 air quality data from each of the simulation 

years included in the analysis (2007 and 2009) from population-oriented monitors in 

the assessment location (these are aggregated to form composite monitor values used 

to represent population exposure), and (2) a method for adjusting the air quality data 

to simulate just meeting the existing or alternative suite of O3 standards. (These air 

quality inputs are discussed in more detail in Chapter 4). 

 C-R function(s): which provide an estimate of the relationship between the health 

endpoint of interest and O3 concentrations (for this analysis, C-R functions used were 

applied to urban study areas matching the assessment locations from the 

epidemiological studies used in deriving the functions, in order to increase overall 

confidence in the risk estimates generated - see section 7.3.2). For O3, 

epidemiological studies providing information necessary to specify C-R functions are 

readily available for O3-related health effects associated with short-term exposures 

(Section 7.1.2 describes the role of C-R functions in estimating health risks associated 

with O3). In addition, the Jerrett et al. (2009) study provided a C-R function for 

modeling mortality risks associated with longer-term exposures to O3. 
7-9 

 Population information (baseline health affects incidence and prevalence rates 

and population): The baseline incidence provides an estimate of the incidence rate 

(number of cases of the health effect per year or day, depending on endpoint, usually 

per 10,000 or 100,000 general population) in the assessment location corresponding 

to recent ambient O3 levels in that location. The baseline prevalence rate describes the 

prevalence of a given disease state or conditions (e.g., asthma) within the population 

(number of individuals with the disease state/condition, usually per 10,000 or 100,000 

general population). To derive the total baseline incidence or prevalence per year, this 

rate must be multiplied by the corresponding population number (e.g., if the baseline 

incidence rate is number of cases per year per 100,000 population, it must be 

multiplied by the number of 100,000s in the population) (Section 7.3.3 summarizes 

considerations related to the baseline incidence and prevalence rates and population 

data inputs to the risk assessment). 

In addition to the inputs described above, it is also necessary to specify the spatial extent 

of the study areas that will be modeled. These study areas definitions determine the composition 

of (a) the composite monitor values (which specific set of monitors are used in constructing the 

composite monitor, reflecting the area-wide average across monitors for each study area), (b) the 

specific set of effect estimates that will be used (matching the study areas to the specific set of 

effect estimates in the epidemiological studies being used to support modeling of endpoints), (c) 

the baseline incidence data and (d) the population demographic (count) data for each study area. 

As mentioned earlier, for this HREA we have modeled 12 urban study areas and have used the 

CBSA spatial definition to specify the extent of each of these urban areas (see section 7.3.1 for 

additional details on study area selection). 
7-10 

Figure 7-1. Flow Diagram of Risk Assessment for Short-term Exposure Studies. 
7-11 

This risk assessment was implemented using the EPA’s Environmental Benefits Mapping 

and Analysis Program (BenMAP, version 4.0) (U.S. EPA, 2013b). This GIS-based computer 

program draws upon a database of population, baseline incidence/prevalence rates and effect 

coefficients to automate the calculation of health impacts. For this analysis, the standard set of 

effect coefficients and health effect incidence data available in BenMAP has been augmented to 

reflect the latest studies and data available for modeling O3 risk. EPA has traditionally relied 

upon the BenMAP program to estimate the health impacts avoided and economic benefits 

associated with adopting new air quality rules. For this analysis, EPA used the model to estimate 

O3-related risk for the suite of health effects endpoints described in section 3.2. There are three 

primary advantages to using BenMAP for this analysis, as compared to the procedure for 

estimating population risk followed in the last review. First, once we have configured the 

BenMAP software for this particular O3 analysis, the program can produce risk estimates for an 

array of modeling scenarios across a large number of urban areas. Second, the program can more 

easily accommodate a variety of sensitivity analyses. Third, BenMAP allowed us to complete the 

national assessment of O3 mortality described in Chapter 8, which plays in important role in 

assessing the representativeness of the urban study area analysis. 

7.1.2 Calculating Ozone-Related Health Effects Incidence 

The C-R functions used in the risk assessment are empirically estimated associations 

between average ambient concentrations of O3 and the health endpoints of interest (e.g., 

mortality, hospital admissions (HA), emergency department (ED) visits). This section describes 

the basic method used to estimate changes in the incidence of a health endpoint associated with 

changes in O3, using a “generic” C-R function of the most common functional form. 

Although some epidemiological studies have estimated linear C-R functions and some 

have estimated logistic functions, most of the studies used a method referred to as “Poisson 

regression” to estimate exponential (or log-linear) C-R functions in which the natural logarithm 

of the health endpoint is a linear function of O3: 

 x y Be  (1) 

where x is the ambient O3 level, y is the incidence of the health endpoint of interest at O3

level x, β is the coefficient relating ambient O3 concentration to the health endpoint, and B is the 

incidence at x=0, i.e., when there is no ambient O3. The relationship between a specified ambient 

O3 level, x0, for example, and the incidence of a given health endpoint associated with that level 

(denoted as y0) is then 

 0

0

x y Be   (2) 
7-12 

Because the log-linear form of a C-R function (equation (1) is by far the most common 

form, we use this form to illustrate the “health impact function” used in the O3 risk assessment. 

If we let x0 denote the baseline (upper) O3 level, and x1 denote the lower O3 level, and y0

and y1 denote the corresponding incidences of the health effect, we can derive the following 

relationship between the change in x, Δx= (x0- x1), and the corresponding change in y, Δy, from 

equation (1).12

  

yyy y e x    ( ) [ ]. 01 0 1  (3) 

Alternatively, the difference in health effects incidence can be calculated indirectly using 

relative risk. Relative risk (RR) is a measure commonly used by epidemiologists to characterize 

the comparative health effects associated with a particular air quality comparison. The risk of 

mortality at ambient O3 level x0 relative to the risk of mortality at ambient O3 level x1, for 

example, may be characterized by the ratio of the two mortality rates: the mortality rate among 

individuals when the ambient O3 level is x0 and the mortality rate among (otherwise identical) 

individuals when the ambient O3 level is x1. This is the RR for mortality associated with the 

difference between the two ambient O3 levels, x0 and x1. Given a C-R function of the form 

shown in equation (1) and a particular difference in ambient O3 levels, Δx, the RR associated 

with that difference in ambient O3, denoted as RRΔx, is equal to eβΔx. The difference in health 

effects incidence, Δy, corresponding to a given difference in ambient O3 levels, Δx, can then be 

calculated based on this RRΔx as: 

( ) [1 (1/ )] 0 1 0 RR x y y y y       . (4) 

Equations (3) and (4) are simply alternative ways of expressing the relationship between 

a given difference in ambient O3 levels, Δx > 0, and the corresponding difference in health 

effects incidence, Δy.13 These health impact equations are the key equations that combine air 

quality information, C-R function information, and baseline health effects incidence information 

to estimate ambient O3 health risk. 

 

12 If Δx < 0 – i.e., if Δx = (x1- x0) – then the relationship between Δx and Δy can be shown to be 

( ) [ 1]   1  0  0  x y y y y e  . If Δx < 0, Δy will similarly be negative. However, the magnitude of Δy will be the 

same whether Δx > 0 or Δx < 0 – i.e., the absolute value of Δy does not depend on which equation is used. 13 When calculating total risk associated with a specific air quality scenario, Δx is the total O3 concentration 

associated with a given study area (as noted earlier in section 7.1.1, we are not incorporating thresholds, such as 

LMLs into this analysis). 
7-13 

7.2 AIR QUALITY CONSIDERATIONS 

Air quality data are discussed in detail in Chapter 4 of this report. Here we describe those 

air quality considerations that are directly relevant to the estimation of health risks in the 

epidemiology based portion of the risk assessment. As described in section 7.1.1, the risk 

assessment uses composite (area-wide average) monitor values derived for each urban study area 

as the basis for characterizing population exposure in modeling risk. The use of composite 

monitors reflects consideration for the way ambient O3 data are used in the epidemiological 

studies providing the C-R functions (see section 7.1.1). For the short-term exposure related 

health endpoints, the composite monitor values derived for this analysis include hourly timeseries for each study area (where the O3 value for each hour is the average of measurements 

across the monitors in that study area reporting values for that hour). Once these composite 

monitor hourly time series are constructed, we can then extract short-term peak O3 metrics 

needed to model specific health effects endpoints. For short-term O3-attributable endpoints, 

reflecting consideration for available evidence in the published literature (see section 7.3.2), we 

have focused the analysis on short-term peak O3 metrics including 1-hr maximum, 8-hr mean 

and 8-hr maximum. The 24-hr average has been deemphasized for this analysis, although it is 

still used in risk modeling when use of C-R functions based on this metric allow us to cover a 

specific health effect endpoint/location of particular interest (see section 7.3.2).14

For modeling mortality risk associated with long-term O3-attributable we construct 

seasonally-averaged maximum hourly O3 values (see section 7.3.2). The derivation of composite 

monitor distributions used in modeling this health effect endpoint is different than that used for 

short-term O3-attributable endpoints. Specifically, for the long-term O3-attributable endpoint we 

first construct the seasonally-averaged peak O3 metric for each monitor within a given study area 

and then average those monitor-specific metric values together to generate a single composite 

value to use in generating risk estimates for that study area. 

In applying effect estimates obtained from epidemiological studies we attempted to 

match the modeling period (e.g. O3 monitoring season) associated with each epidemiology study. 

This increases overall confidence in the risk compared with using a single more generalized 

specification of the modeling period. As discussed earlier, we modeled all health effect endpoints 

for the core analysis using a CBSA-based study area. The use of the CBSA-based study areas 

addresses potential bias that would have occurred had we focused the risk assessment on the 

smaller core urban study areas (see section 7.1.1). Table 7-1 identifies (a) the counties associated 

with the CBSA definition for each of the 12 urban study areas, (b) the number of O3 monitors 

 

14 In order to provide estimates of respiratory-related hospital admission for Los Angeles, we did include a C-R 

function based on Linn et al., 2000, which utilizes a 24-hr average exposure metric. 
7-14 

associated with each CBSA (and a flag for whether the design value monitor is contained within 

the CBSA), (c) the number of monitors associated with the smaller Smith et al., 2009-based 

study areas, and (d) the specific O3 modeling period for each study area. A map showing the 

counties and monitors for these 12 urban areas can be found in Chapter 4 (Figure 4-5, Section 

4.3.2.2). 

Table 7-1. Information on the 12 Urban Study Areas in the Risk Assessment. 

Study Area 

Counties Associated with the CBSA 

Definition 

# of O3

Monitors 

within the 

CBSAa Required O3 Monitoring Season

Atlanta 

Barrow, Bartow, Butts, Carroll, Cherokee 

Clayton, Cobb, Coweta, Dawson, DeKalb, 

Douglas, Fayette, Forsyth, Fulton, 

Gwinnett, Haralson, Heard, Henry, 

Jasper, Lamar, Meriwether, Newton, 

Paulding, Pickens, Pike, Rockdale, 

Spalding, Walton 

13 (3) March - October 

Baltimore Anne Arundel, Baltimore, Carroll, Harford, 

Howard, Queen Anne's, Baltimore 7 (1) April - October 

Boston Essex, Middlesex, Norfolk, Plymouth, 

Suffolk, Rockingham, Strafford 11* (2) April - September 

Cleveland Cuyahoga, Geauga, Lake, Lorain, Medina 10* (4) April - October 

Denver 

Adams, Arapahoe, Broomfield, Clear 

Creek, Denver, Douglas, Elbert, Gilpin, 

Jefferson, Park 

16 (6) March - September 

Detroit Lapeer, Livingston, Macomb, Oakland, 

St. Clair, Wayne 8 (4) April - September 

Houston 

Austin, Brazoria, Chambers, Fort Bend, 

Galveston, Harris, Liberty, Montgomery, 

San Jacinto, Waller 

22 (17) January - December 

Los Angeles Los Angeles, Orange 21* (17) January - December 

New York 

Bergen, Essex, Hudson, Hunterdon, 

Middlesex, Monmouth, Morris, Ocean, 

Passaic, Somerset, Sussex, Union, 

Bronx, Kings, Nassau, New York, 

Putnam, Queens, Richmond, Rockland, 

Suffolk, Westchester, Pike 

22 (7) April - October 

Philadelphia 

New Castle, Cecil, Burlington, Camden, 

Gloucester, Salem, Bucks, Chester, 

Delaware, Montgomery, Philadelphia 

15 (4) April - October 

Sacramento El Dorado, Placer, Sacramento, Yolo 17 (8) January - December 

St. Louis 

Bond, Calhoun, Clinton, Jersey, 

Macoupin, Madison, Monroe, St. Clair, 

Franklin, Jefferson, Lincoln, St. Charles, 

St. Louis, Warren, Washington, St. Louis 

17 (2) April - October 

a

 column presents the number of monitors within each CBSA, whether the design value falls outside of the CBSA 

(denoted with an “*”) and the number of monitors within the smaller Smith et al., 2009-based study area (in 

parenthesis).
7-15 

We estimate risk associated with recent O3 conditions as well as risk associated with 

simulating just meeting the existing and alternative standards. While the derivation of composite 

monitor hourly O3 distributions (and associated peak exposure metrics) for recent conditions is 

relatively straightforward, the generation of these estimates for the scenarios of just meeting the 

existing and alternative standards is more complex. The procedures for adjusting air quality to 

just meet the existing and alternative O3 standards are presented in Chapter 4 and Chapter 4 

appendices. 

Summary statistics for the air metrics used in modeling risk for each of the 12 urban 

study areas under recent conditions and for air quality adjusted to just meets the existing and 

alternative standard levels are presented in Chapter 4 (see section 4.3.3.2, Figures 4-9 (2007) and 

4-10 (2009)). 

7.3 SELECTION OF MODEL INPUTS AND ASSUMPTIONS 

7.3.1 Selection of Urban Study Areas 

This analysis focuses on modeling risk for a set of urban study areas, reflecting the goal 

of providing risk estimates that have greater overall confidence due to the use of locationspecific data when available for these urban locations. In addition, given the greater availability 

of location-specific data, a more rigorous evaluation of the impact of uncertainty and variability 

can be conducted for a set of selected urban study areas than would be possible for a broader 

regional or national-scale analysis. We considered the following factors in selecting the 12 urban 

study areas included in this analysis: 

 Air Quality Data: An urban area has reasonably comprehensive monitoring data for 

the period of interest (2006-2010) to support the risk assessment. This criterion was 

evaluated qualitatively by considering the number of monitors within the CBSA of 

the prospective urban areas. Locations with one or two monitors would be excluded 

since they had relatively limited spatial coverage in characterizing O3 levels. 

 Elevated Ambient O3 Levels: Because we are interested in evaluating the potential 

magnitude of risk reductions associated with just meeting the existing and alternative 

O3 standard levels, we focus on study areas with elevated ambient O3 levels at or 

above the existing standard, such that just meeting alternative O3 standard levels 

would result in some degree of risk reduction. 

 Location-specific C-R Functions: Given the health endpoints selected for inclusion 

in the analysis (see section 7.3.2), there are epidemiological studies of sufficient 

quality available for these urban study areas to provide the C-R functions necessary 

for modeling risk. This criterion primarily applies to short-term epidemiological 

studies since the associated health effect endpoints are the primary focus of the 
7-16 

HREA. Short-term O3-attributable epidemiological studies often include city-specific 

effect estimates, and in some cases are multi-city studies that provide estimates for 

multiple cities. 

 Baseline Incidence Rates and Demographic Data: The required urban area-specific 

baseline incidence rates and population data are available for a recent year for at least 

one of the health endpoints. 

 Geographic Heterogeneity: Because O3 distributions and population characteristics 

vary geographically across the U.S., we selected urban study areas to provide 

coverage for regional variability in factors related to O3 risk including variability in 

the spatial pattern of O3 in the urban area, population exposure (differences in 

residential housing density, air conditioning use and commuting patterns), 

demographic characteristics (baseline incidence rates, socio-economic status) and 

variability in effect estimates. The degree to which the set of urban study areas 

provided coverage for regional differences across the U.S. in many of these O3 riskrelated factors was evaluated as part of the representativeness analysis presented in 

Chapter 8. 

Application of the above criteria resulted in the selection of 12 urban study areas for 

inclusion in the risk assessment including: 

 Atlanta,	GA	

 Baltimore,	MD	

 Boston,	MA	

 Cleveland,	OH	

 Denver,	CO	

 Detroit,	MI	

 Houston,	TX	

 Los	Angeles,	CA	

 New	York,	NY	

 Philadelphia,	PA	

 Sacramento,	CA	

 St.	Louis,	MO	

The specific set of counties used in defining each of the 12 urban study areas based on 

the CBSA is presented in Table 7-1. 
7-17 

7.3.2 Selection of Epidemiological Studies and Specification of Concentration-Response 

Functions 

Once the set of health effect endpoints to be included in the risk assessment has been 

specified, the next step was to select the set of epidemiological studies that will provide the 

effect estimates and model specifications used in the C-R functions. This section describes the 

approach used in completing these tasks and presents a summary of the epidemiological studies 

and associated C-R functions specified for use in the risk assessment. 

In Chapter 2, section 2.5 we identified the set of health effect categories and associated 

endpoints to be included in this assessment, based on review of the evidence provided in the O3

ISA (U.S. EPA, 2013a). The selection of specific health effect endpoints to model within a given 

health effect endpoint category is an iterative process involving review of both the strength of 

evidence (for a given endpoint) as summarized in the O3 ISA together with consideration for the 

available epidemiological studies supporting a given endpoint and the ability to specific key 

inputs needed for risk modeling, including effect estimates and model forms. Ultimately, 

endpoints are only selected if (a) they are associated with an overarching effect endpoint 

category selected for inclusion in the risk assessment and (b) they have sufficient 

epidemiological study support to allow their modeling in the risk assessment. Health effect 

endpoints selected for inclusion in HREA include: 

Short-term O3-attributable effects: 

 Mortality (likely to be a causal relationship) 

o All-cause (non-accidental) 

o Cardiovascular 

o Respiratory 

 Respiratory effects (causal relationship) 

o ED (for asthma, wheeze, all respiratory symptoms) 

o HA (for COPD, asthma, all	respiratory)15

o Respiratory	symptoms	

 

15 Regarding chronic obstructive pulmonary disease (COPD)-related HA, the O3 ISA states that “Although limited in 

number, both single- and multi-city studies consistently found positive associations between short-term O3

exposures and asthma and COPD hospital admissions.” (U.S. EPA, 2013a, p. 6-128). It is also important to point 

out that when modeling of COPD-related HA is limited to the summer months (as was done for the HREA), 

available effect estimates have tighter confidence intervals and are generally positive, which increases overall 

confidence in the resulting risk estimate (see U.S. EPA, 2013a, Figure 6-19). 
7-18 

Long-term O3-attributable effects:

 Respiratory effects, focusing on respiratory-related mortality (likely causal 

relationship).16

We selected epidemiological studies to support modeling of the health effect endpoints 

listed above by applying a number of criteria including:17

 The study was peer-reviewed, evaluated in the O3 ISA, and judged adequate by EPA 

staff for purposes of inclusion in the risk assessment. We considered the following 

criteria: whether the study provides C-R relationships for locations in the U.S., 

whether the study has sufficient sample size to provide effect estimates with a 

sufficient degree of precision and power, and whether adequate information is 

provided to characterize statistical uncertainty. 

 Preference for multicity studies given that they typically have greater power and 

reflect patterns of O3 related health effects over a range of urban areas (and regions) 

which can display variability in key risk-related factors such as exposure 

measurement error. In the case of short-term O3-attributable mortality, we also 

favored those multi-city studies for which we could obtain Bayesian-adjusted cityspecific estimates from the study authors, since these incorporate both city-specific 

effect information with information from the broader array of cities included in the 

study. In those instances where we did not have multi-city studies (e.g., with many of 

the short-term respiratory-related morbidity endpoints) we use single-city studies. 

 The study design is considered robust and scientifically defensible, particularly in 

relation to methods for covariate adjustment, including treatment of confounders, as 

well as treatment of effect modifiers. For example, if a given study used ecologicaldefined variables (e.g., smoking rates) as the basis for controlling for confounding, 

concerns may be raised as to the effectiveness of that control. 

 

16 The O3 ISA classifies long-term O3-attributable respiratory health effects, including respiratoryrelated mortality, as having a likely causal classification. By contrast, it classifies long-term O3-

attributable total mortality as having a suggestive of a causal relationship classification (O3

ISA, Chapter 1). We have focused on modeling long-term O3-attributable respiratory-related 

mortality given the greater support for this health endpoint relative to total mortality. 

17 In addition to the criteria listed here, we also attempted to include studies that provide coverage for populations 

considered particularly at-risk for a particular health (e.g., children, individuals with preexisting disease). 

However, a study would have to meet the criteria listed here (in addition to providing coverage for an at-risk 

population) in order for that study to be used to derive C-R functions. 
7-19 

 The study is not superseded by another study (e.g., if a later study is an extension or 

replication of a former study, the later study would effectively replace the former 

study), unless the earlier study has characteristics that are clearly preferable (e.g., 

inclusion of co-pollutants models, or use of a peak exposure metric of interest). 

We applied the above criteria and selected the set of epidemiological studies presented in 

Table 7-2 for use in specifying C-R functions (Table 7-2 also describes elements of the C-R 

functions specified using each epidemiological study, as discussed below). 

As part of methods refinement for this risk assessment, we considered studies that 

utilized more sophisticated and potentially representative exposure surrogates in characterizing 

population exposure (e.g., using population-weighted O3 monitor values instead of equallyweighted monitors, linking exposures in individual counties or U.S. Census tracts to the nearest 

monitor, rather than using a composite monitor value to represent the entire study area). 

However, analysis conducted by EPA demonstrated that use of the simpler composite monitor 

approach (as used for other short-term O3-attributable morbidity endpoints) generated risk 

estimates that were very close to those generated using the population-weighted O3 metric. 

Therefore, in order to conserve time and resources, we modeled this endpoint using the more 

generalized composite monitor-based metric. And finally, a number of the long-term O3-

attributable morbidity studies originally considered for modeling this endpoint category did 

involve more complex O3 metrics (e.g., Akinbami et al., 2010; Meng et al., 2010; Moore et al., 

2008). However, limitations in the study-level data required to support risk assessment prevents 

us at this point from completing a quantitative risk assessment for this category of health 

endpoints with a reasonable degree of confidence.18

Based on additional evaluation of the literature, we have substituted Smith et al. (2009) 

for Bell et al. (2004) as a source of Bayes-adjusted city-specific effect estimates to support 

modeling short-term O3-attributable mortality. This decision reflects a number of factors. Smith 

et al. (2009) includes a wider range of simulations exploring sensitivity of the mortality effect to 

different model specifications including (a) regional versus national Bayes-based adjustment, (b) 

co-pollutants models considering PM10, and (c) all - year versus O3-season based estimates. This 

is contrasted with the Bell et al. (2004) study which does not provide this degree of model 

exploration. In obtaining the city-specific Bayes-adjusted effect estimates for the Smith et al., 

 

18 However, these limitations do not prevent the use of this evidence from informing consideration of the levels of 

exposure at which specific types of health effects may occur (i.e., the evidence analysis, which is an important 

aspect of the O3 NAAQS review). Rather, these limitations only prevent the quantitative estimation of risk with a 

reasonable degree of confidence. 
7-20 

2009 study from the study authors, we were provided with estimates reflecting this range of 

alternative model specifications which allowed us to incorporate them into both the core and 

sensitivity analysis portions of the HREA (see section 7.4.3). In addition, the Smith et al. (2009) 

study does not use the trimmed mean approach employed in the Bell et al. (2004) study in 

preparing O3 monitor data. We have a number of concerns regarding the trimmed mean approach 

including (1) the potential loss of temporal variation in the data when the approach is used (this 

could impact the size of the effect estimate) and (2) a lack of complete documentation for the 

approach which prevents us from fully reviewing the technique and using it in preparing O3 

metrics for the HREA. Given these concerns, we view it as advantageous that the Smith et al. 

(2009) study does not use the trimmed mean approach. 

With the exception of the trimmed mean approach, the Smith et al. (2009) study was 

intended to reproduce the results of the Bell et al. (2004) analysis. Thus, the core risk results 

based on Smith et al. (2009) are functionally comparable to the 1st draft HREA estimates based 

on Bell et al. (2004), while the alternative models provided in Smith et al. (2009) allow for an 

expanded set of sensitivity analyses. The comparability of the Smith et al. (2009) and Bell et al. 

(2004) estimates is confirmed by the graphical comparison in Smith et al. (2009) of mortality 

effect estimates (for the 24-hr O3 metric) with matching effect estimates from Bell et al. (2004). 

This comparison demonstrates the close match of the two studies (for this particular scenario). 

Reflecting the points made above, in modeling short-term O3-attributable mortality, we 

have included a core analysis based on the national-Bayesian adjusted city-specific effect 

estimates (reflecting the full O3 monitoring period in each city) obtained from Smith et al. 

(2009). As sensitivity analyses, we have included effect estimates obtained from Smith et al. 

(2009) which reflect application of co-pollutants models (including PM10), Bayes adjustment 

using a regional prior,19 and a shorter fixed O3 measurement period (April-October). In the 1st

draft HREA, we had also included national Bayes-adjusted effect estimates (reflecting a fixed 

June-August period) obtained from Zanobetti and Schwartz (2008) as part of the core analysis. 

However, here we decided to include these as part of the sensitivity analysis here because these 

effect estimates cover a more limited warm-weather period and consequently will generate only 

partial characterizations of mortality risk (since they exclude risk occurring during the nonsummer months). 

We have also included estimates of respiratory-related mortality associated with longterm O3 exposures (summer season mean of daily maximum 1-hr O3) based on effect estimates 

obtained from Jerrett et al. (2009). The decision to model long-term O3-attributable mortality 

 

19 With application of a regional prior within Bayesian adjustment, city-specific effect estimates are adjusted 

towards the regional value rather than a national value as is the case with the application of a national prior. 
7-21 

reflects consideration for evidence supporting a likely to be a causal relationship for long-term 

O3-attributable respiratory effects, including mortality (O3 ISA, section 2.5.2). The Jerrett et al. 

(2009) study was the first study to explore the relationship between long-term O3 exposure and 

respiratory mortality (rather than focusing on cardiopulmonary mortality). Jerrett et al. (2009) 

does have a number of strengths including (a) the study is based on the 1.2 million participant 

American Cancer Society cohort drawn from all 50 states, DC, and Puerto Rico (included O3

data from 1977 [5 years before enrollment in the cohort began] to 2000); (b) inclusion of copollutant models that controlled for PM2.5; and (c) exploration of the potential for a threshold 

concentration associated with the long-term mortality endpoint. However we also recognize a 

few factors which impact overall interpretation of the long-term exposure-related respiratory 

mortality estimates based on this study. First, while the Jerrett et al., (2009) study is a relatively 

strong study in terms of overall design, it is a single study for this particular health endpoint 

which means that the underlying support for the quantitative risk estimation for this endpoint is 

limited in comparison with other endpoints modeled (e.g., short-term exposure-related mortality 

risk that uses numerous studies). In addition, there is uncertainty about the existence and location 

of a threshold in the C-R function relating mortality and long-term O3 concentrations, and that 

uncertainty may have a large impact on our quantitative risk estimates. 

The exploration of potential thresholds presented in the Jerrett et al., (2009) study 

deserves additional discussion.20 In their memo clarifying the results of their study (see Sasser, 

2014), the authors note that in terms of goodness of fit, long-term health risk models including 

O3 clearly performed better than models without O3, indicating the improved predictions of 

respiratory mortality when O3 is included. In exploring different functional forms, they report 

that the model including a threshold at 56 ppb had the lowest log-likelihood value of all models 

evaluated (i.e., linear models and models including thresholds ranging from 40-60 ppb), and thus 

provided the best overall statistical fit to the data. However, they also note that it is not clear 

whether the 56 ppb threshold model is a better predictor of respiratory mortality than when using 

a linear (no-threshold) model for this dataset. Using one statistical test, the model with a 

threshold at 56 ppb was determined to be statistically superior to the linear model. Using another, 

more stringent test, none of the threshold models considered were statistically superior to the 

linear model. Under the less stringent test, although the threshold model produces a statistically 

superior prediction than the linear model, there is uncertainty about the specific location of the 

 

20 The approach we developed to explore the potential for thresholds related to long-term exposure-related mortality 

was presented in a memorandum to CASAC which was also released to the public (Sasser, 2014). That 

memorandum describes additional data obtained from the authors of Jerrett et al. (2009) to support modeling of 

potential thresholds and also lays out our proposed approach for exploring the impact of potential thresholds on 

estimates of long-term exposure-related mortality. 
7-22 

threshold, if one exists. This is because the confidence intervals on the model predictions 

indicate that a threshold could exist anywhere from 0 to 60 ppb. The authors conclude that 

considerable caution should be exercised in using any specific threshold, particularly when the 

more stringent statistical test indicates there is no significantly improved prediction. Based on 

this additional information from the authors (Sasser, 2014), we have chosen to reflect the 

uncertainty about the existence and location of a potential threshold by estimating mortality 

attributable to long-term O3 exposures using a range of threshold-based effect estimates as 

sensitivity analyses. Specifically, we generate additional long-term risk results using unique risk 

models that include a range of thresholds from 40 ppb to 60 ppb in 5 ppb increments, while also 

including a model with a threshold equal to 56 ppb, which had the lowest log likelihood value for 

all models examined.21

Other limitations associated with the Jerrett et al. (2009) study include possible exposure 

misclassification and uncontrolled confounding by temperature, which are endemic to most longterm epidemiological studies. It is also important to note that, while Jerrett et al. (2009) found 

negative associations between O3 exposure and cardiovascular mortality when controlling for 

PM2.5, null or negative associations for O3 are consistent with the evidence that PM2.5 is the 

pollutant most strongly associated with cardiovascular disease (U.S. EPA, 2009). 

We based the core estimate for long-term exposure-related mortality on a co-pollutant 

model (with PM2.5) obtained from Jerrett et al. (2009). This reflects the observation that the 

seasonal average metrics used in the long-term exposure-related mortality are not very sensitive 

to the reduced number of days with co-pollutant monitoring, and as such it is appropriate to 

include the co-pollutant model as the core estimate. We also include three sensitivity analyses for 

long-term O3-attributable respiratory mortality including: (a) application of regionallydifferentiated effect estimates (although these do not include a co-pollutants model 

specification), (b) application of a single pollutant (O3-only) national-based effect estimate and 

(c) application of the suite of effect estimates reflecting potential thresholds at 40, 45, 50, 55, 56 

and 60 ppb (effect estimates for both the core and sensitivity analyses are presented in Appendix 

7A). 

The effect estimates used in modeling long-term O3-attributable mortality (see Table 7-2) 

utilize a seasonal average of peak (1-hr maximum) measurements. These long-term exposure 

metrics can be viewed as long-term exposures to daily peak O3 over the warmer months, as 

compared with annual average levels such as are used in long-term PM exposure calculations. 

 

21 There is a separate effect estimate (and associated standard error) for each of the fitted threshold models estimated 

in Jerrett et al. (2009). As a result, the sensitivity of estimated mortality attributable to long-term O3

concentrations is affected by both the assumed threshold level (below which there is no effect of O3) and the effect 

estimate applied to O3 concentrations above the threshold. 
7-23 

This increases the need for care in interpreting these long-term O3-attributable mortality 

estimates together with the short-term O3-attributable mortality estimates, in order to avoid 

double counting. It is also important to keep in mind that our estimates of short-term O3-

attributable mortality are for all-causes, while estimates of long-term O3-attributable mortality 

are focused on respiratory-related mortality. This further limits the ability to compare estimates 

of long-term and short-term exposure related mortality. 

Once the set of epidemiology studies described above was selected, the next step was to 

specify C-R functions for use in the risk assessment. Several factors were considered in 

identifying the effect estimates and model forms used in specifying C-R functions for each 

endpoint. These factors are described below: 

 Ozone Exposure Metric: In the risk assessment performed for the previous O3

NAAQS review, for short-term exposure, we included C-R functions based on 24-hr 

averages as well as a number of peak O3 measurements. However, given that the 

existing O3 NAAQS standard uses an 8-hr average form and given that many of the 

clinical studies involving O3 also utilize shorter exposures (on the order of 2 to 8 

hours – see O3 ISA, section 6.2.1.1), we wanted to see if the latest epidemiological 

studies for O3 also supported use of an 8-hr averaging time in modeling risk. Several 

epidemiological studies completed since the last review provide limited support for 

stronger associations between health endpoints and peak O3 metrics (i.e., 1-hr 

maximum, 8-hr maximum and 8-hr means) relative to 24-hr averages. Specifically, a 

study of respiratory ED visits in Atlanta (Darrow et al., 2011) found stronger 

associations with peak metrics (including 1-hr and 8-hr maximum measurements) 

compared with 24-hr averages (see O3 ISA, section 6.2.7.3 and Figure 6-17, U.S. 

EPA, 2013a). Similarly, for short-term exposure-related mortality, there are also a 

limited number of epidemiologic studies that have compared mortality associations 

with peak O3 metrics and the 24-hr average metric. Although the O3 ISA recognizes 

that 24-hr exposure metrics when used in time series studies may result in smaller risk 

estimates, ultimately it concludes that “Overall, the evidence from time-series and 

panel epidemiologic studies does not indicate that one exposure metric is more 

consistently or strongly associated with mortality or respiratory-related health effects” 

(U.S. EPA, 2013a, section 2.5.4.2). Based on consideration for the evidence 

summarized in the O3 ISA, we have decided to focus on peak exposure metrics 

because of the limited evidence that these metrics may be associated with higher risk 

estimates relative to the 24-hr exposure metric. However, we recognize that, as 

summarized in the O3 ISA, there is only weak support for differentiating between 

these two categories of short-term exposure metric.
7-24 

Table 7-2. Overview of Epidemiological Studies Used in Specifying C-R Functions. 

Epidemiological 

Study 

 (stratified by O3-

attributable 

health 

endpoints) 

Health 

Endpoints 

Location 

(urban 

study 

area(s) 

covered) 

Exposure Metric 

(and modeling 

period) Additional Study Design Details Notes Regarding Applica

Short-term O3-attributable mortality Smith et al., 2009 Non-accidental, 

respiratory, cardiovascular 

95 large urban communities (provides coverage for all 12 urban study areas) 

24-hr avg, 8-hr max, 1-hr max. April through October and all year 

Adjusting for time-varying confounders (PM, weather, seasonality). Lag structure included 0, 1, 2 and day 3 lag as well as 0-6 day distributed lag. Age range: all ages. 

Focused on the 8-hr max-basefor the HREA (see text discussObtained Bayes-adjusted city-sfor non-accidental all-cause mo(personal communication, Dr. January 15, 2013) reflecting co

following modeling elements: (national-prior Bayes model adjpollutant versus co-pollutants (

full monitoring period versus suOctober). For the core analysissingle pollutant (O3-only) mode

monitoring period. The co-pollu

was included as a sensitivity a7.4.3). 

Zanobetti and Schwartz (2008) 

Non-accidental, respiratory, cardiovascular 

48 U.S. cities (provides coverage for the 12 urban study areas) 

8-hr max. JuneAugust Effect controlled for season, day of week, and temperature. Lag structure 

included 0-3 day, 0-20 and 4-20 day). Age range: all ages 

Obtained Bayes-adjusted city-sfor non-accidental, respiratory Dr. Zanobetti (personal commuZanobetti, January 5, 2012). Treflect a 0-3 day distributed lag mean O3 levels measured betw

Estimates were generated for ethis constrained warm-season 

Short-term O3-attributable morbidity - HA for respiratory effect) Medina-Ramon et al., 2006. 

HA: COPD, pneumonia 

36 cities (provides coverage for all 12 urban study areas) 

8-hr mean. warm (May-September), cool (OctoberApril), all year 

Distributed lag (0-1 day). Age range: ≥ 65yrs. Controlled for day of the week and weather (including temperature). 

Generated risk estimates baseCOPD only (May-September). 

Linn et al., 2000 HA: 

unscheduled for pulmonary illness 

LA only 24-hr mean, LA O3

season (all year), winter, spring, summer and autumn 

Lag 0. Age range: all ages. Used subgroup analysis to explore the effect of temporal variation, weather and autocorrelation on O3 effect. 

Included effect estimate based summer) since this provided adin L.A. Modeled using air quali

Lin et al., 2008 HA: respiratory 

disease 

NY State (used to cover NYC) 

1-hr max (for 10am-6pm interval), warm season (AprilOctober) 

Lag 0, 1, 2, 3. Age range: <18yrs. Models adjusted for the confounding effects of demographic characteristics, particulate matter (PM10), meteorological conditions, 

Used 1-hr max metric applied t

season for NY (April-October). 
7-25 

Epidemiological 

Study 

 (stratified by O3-

attributable 

health 

endpoints) 

Health 

Endpoints 

Location 

(urban 

study 

area(s) 

covered) 

Exposure Metric 

(and modeling 

period) Additional Study Design Details Notes Regarding Applica

day of the week, seasonality, longterm trends, and different lag periods of exposure. 

Katsouyanni et al. (2009) 

HA: cardiovascular disease, chronic obstructive pulmonary disease, pneumonia, all respiratory 

14 cities (provides coverage for Detroit only) 

1-hr max. Summer only and all year 

Lag 0-1 day. Age range: ≥ 65yrs. 

Models accounted for seasonal patterns, but also, for weekend and vacation effects, and for epidemics of respiratory disease. The data were also analyzed to detect potential thresholds in the concentration–response relationships. 

C-R function applied only for aUsed June-August-based com

Silverman et al. (2010) 

HA: asthma (ICU and nonICU) 

NYC 8-hr max. Warm 

season (AprilAugust) 

Includes control for PM2.5. Lag 0-1 

day. Age range: children 6-18yrs. The model adjusted for temporal trends, weather, and day of the week. 

Applied C-R function (for O3 an

PM2.5) to the city-specific O3 se

longer than the modeling perio

Short-term O3-attributable morbidity– ED and ER visits (respiratory) Ito et al,(2007) ED: asthma NYC 8-hr max. Warm 

season (AprilSeptember) 

Includes models controlling for SO2, 

NO2, CO and PM2.5. Lag: 0, 1, and 

distributed lag (0-1 day). Age range: all ages. Model adjusts for temporal trends, weather terms, day-of-week and other pollutants. 

Applied C-R functions (for O3 a

for listed pollutants) to the city-

NY (slightly longer than the mostudy). 

Tolbert et al. (2007) 

ED: all respiratory 

Atlanta 8-hr max. Summer 

(March-October) 

Includes models controlling for NO2, 

CO, PM10, and NO2/ NO2. Age range: 

all ages. Model controls for temporal trends, temperature, other pollutants. 

Applied C-R functions (for O3 a

for listed pollutants) to the city-

Atlanta. 

Strickland et al. (2010) 

ER: respiratory Atlanta 8-hr max (based on 

population weighted average across monitors). Warm season (May to October) and cool (November to April) 

Lag: average of 0-2 day, distributed lag 0-7 day. Age range: 5-17yrs. Model controls for seasonal trends and meteorology. 

Included effect estimates baseand used composite monitor va

season. 

Darrow et al. (2011) 

ED: all respiratory 

Atlanta 8-hr max, 1-hr max, 

2-4hr avg for summer (MarchOctober). 

Lag: 1day. Age range: all ages. The study used a time series analysis similar to case-crossover with crossover matching based on daily temperature (rather than day of the week) to provide control for this key risk-related factor. 

Used city-specific O3 season-b

values. 
7-26 

Epidemiological 

Study 

 (stratified by O3-

attributable 

health 

endpoints) 

Health 

Endpoints 

Location 

(urban 

study 

area(s) 

covered) 

Exposure Metric 

(and modeling 

period) Additional Study Design Details Notes Regarding Applica

Short-term O3-attributable morbidity – respiratory symptoms Gent et al. (2003) Respiratory 

symptoms: wheeze, persistent cough, chest tightness, shortness of breath 

Springfield, MA (study used to cover Boston) 

1-hr max, 8-hr max Lag: 0 and 1 day. Age range: 

asthmatic children <12 yrs. Model adjusted for temperature. 

Included effect estimates for don both 8-hr max and 1-hr max O3 season composite monitor v

study area (which focuses on Snorthern portion of ConnecticuBoston. However, we are willinassociated with using effect esto provide coverage for Boston providing coverage for this moHowever, there is increased unwith modeling for this endpoint

Long-term O3-attributable respiratory mortality Jerrett et al. (2009) Respiratory, 

cardiovascular, cardiopulmonary 

96 metropolitan statistical areas (provides coverage for all 12 study areas) 

Seasonal average (i.e., Apr-Sep) of the peak daily max1-hr values. 

>30 yrs of age, includes nationallevel and regional effect estimates (only national-level estimate has copollutants modeling considering PM2.5 along with O3). Modeling 

included consideration for a range of potential confounders evaluated at both the ecological level and personal level. 

Included national co-pollutants estimates in core analysis and regional effect estimates and nas sensitivity analyses. Also inreflecting potential thresholds a
7-27 

 Single-and Multi-pollutant Models (pertains to both short-term and long-term 

exposure studies): Epidemiological studies often consider health effects associated 

with ambient O3 using both single-pollutant and co-pollutant models. To the extent 

that any of the co-pollutants present in the ambient air may have contributed to health 

effects attributed to O3 in single pollutant models, risks attributed to O3 may be 

overestimated or underestimated if C-R functions are based on single pollutant 

models. This would argue for inclusion of models reflecting consideration of copollutants. Conversely, in those instances where co-pollutants are highly correlated 

with O3, inclusion of those pollutants in the health impact model can produce unstable 

and statistically insignificant effect estimates for both O3 and the co-pollutants. 

Furthermore, there are often significant differences in sampling frequencies for each 

pollutant included in co-pollutants models, which can lead to a loss of statistical 

power in co-pollutants models (relative to single pollutant models). These last points 

could argue for inclusion of a model based exclusively on O3. Given that single and 

multi-pollutant models each have potential advantages and disadvantages, to the 

extent possible, given available information we have included both types of C-R 

functions in the risk assessment. 

 Multiple Effect Estimates within a Given CBSA-based Study Area: All health 

endpoints, including short-term O3-attributable mortality are modeled using CBSAbased study areas. In the case of both Smith et al. (2009) and Zanobetti and Schwartz 

(2008), these CBSA-based study areas are larger than the study areas used in these 

epidemiological studies to derive effect estimates. Furthermore, for some of the 

CBSA-based urban study areas, several of the smaller study areas evaluated in the 

epidemiological study fall within a single larger CBSA-based study area. For 

example, with the Smith et al. (2009) study, multiple effect estimates are available for 

the CBSA-defined study areas of Los Angeles and New York. Specifically, the Smith 

et al. (2009) study provides separate effect estimates for (a) Santa Anna/Anaheim and 

Los Angeles study areas, both of which fall within the larger CBSA-based Los 

Angeles study area and (b) New York, Jersey City and Newark study areas, all of 

which fall within the larger CBSA-defined New York study area (see Table 7-3). This 

raises the question of how to specify the effect estimate for these larger CBSA-based 

study areas when there are multiple effect estimates available from the 

epidemiological study. For this analysis, in those instances where there are multiple 

effect estimates, we have decided to use the effect estimate that represents the largest 

number of residents within each CBSA-based study area. There is uncertainty 
7-28 

associated with this decision which is discussed both in section 7.4.2 and section 

7.5.3 (as part of the air quality-related sensitivity analysis discussion). 

Table 7-3. CBSA-based Study Areas with Multiple Effect Estimates from the Smith et al. 

(2009) Study 

CBSA 

Study Area 

Smith et al., 

2009 (smaller) 

Study Areas 

with CBSAbased Study 

Areaa

Population 

Totals 

Mortality 

Effect 

Estimate Comments 

New York 

New York, NY 9,100,000 0.0009 New York study area dominates from 

a population standpoint, so that effect 

estimate was chosen to represent the 

entire CBSA. An additional 8.3 

million people live in portions of the 

New York CBSA not covered by the 

Smith et al., 2009 study areas. 

Jersey City, NJ 630,000 0.0001 

Newark, NJ 780,000 0.0005 

Los Angeles 

Santa 

Ana/Anaheim, 

CA 

3,000,000 0.0002 

Los Angeles dominates from a 

population standpoint, so that effect 

estimate was chosen to represent the 

entire CBSA. In this case, the full 

CBSA-based study area is covered by 

the Smith et al., 2009-based subareas. 

Los Angeles, CA 9,800,000 0.0001 

a

 Source: obtained from Dr. Smith (personal communication, Dr. Richard L. Smith, January 15, 2013) 

 Single-city Versus Multi-city Studies: All else being equal, we judge C-R functions 

estimated in the assessment location as preferable to a function estimated in some 

other location, to avoid uncertainties that may exist due to differences associated with 

geographic location. There are several advantages, however, to using estimates from 

multi-city studies versus studies carried out in single cities. Multi-city studies are 

applicable to a variety of settings, since they estimate a central tendency across 

multiple locations. Multi-city studies also tend to have more statistical power and 

provide effect estimates with relatively greater precision than single-city studies due 

to larger sample sizes, reducing the uncertainty around the estimated health 

coefficient. By contrast, single-city studies, while often having lower statistical power 

and varying study designs which can make comparison across cities challenging, 

reflect location-specific factors such as differences in underlying health status, and 

differences in O3 exposure-related factors such as air conditioner use and patterns of 

urban residential density. There is a third type of study design that generates Bayesadjusted city-specific effect estimates, thereby combining the advantages of both cityspecific and multi-city studies. Bayes-adjusted city-specific estimates begin with a 

city-specific effect estimate and shrink that towards a multi-city mean effect estimate 
7-29 

based on consideration for the degree of variance in both estimates. We have elected 

to place greater confidence on these types of Bayesian-adjusted effect estimates when 

they are available. Otherwise, given the advantages for both city-specific and multicity effect estimates, we have used both types when available. 

 Multiple Lag Models: Based on our review of evidence provided in the O3 ISA, we 

believe there is increased confidence in modeling both short-term O3-attributable 

mortality and respiratory morbidity risk based on exposures occurring up to a few

days prior to the health effect, with less support for associations over longer exposure 

periods or effects lagged more than a few days from the exposure (see O3 ISA, section 

2.5.4.3). Consequently, we have favored C-R functions reflecting shorter lag periods 

(e.g., 0, 1 or 1-2 days). With regard to the specific lag structure (e.g., single day 

versus distributed lags), the O3 ISA notes that epidemiological studies involving 

respiratory morbidity have suggested that both single day and multi-day average 

exposures are associated with adverse health effects (see O3 ISA, section 2.5.4.3). 

Therefore, when available both types of lag structures where considered in specifying 

C-R functions for short-term O3-attributable mortality and morbidity. 

 Seasonally-differentiated Effects Estimates: The previous O3 Air Quality Criteria 

Document (AQCD) (published in 2006) concluded that aggregate population timeseries studies demonstrate a positive and robust association between ambient O3

concentrations and respiratory-related hospitalizations and asthma ED visits during 

the warm season (see O3 ISA, section 2.5.3.1). The O3 ISA notes that recent studies of 

short-term O3-attributable respiratory mortality in the U.S. suggest that the effect is 

strengthened in the summer season (O3 ISA, section 2.5.3.1). In addition, many of the 

key epidemiological studies discussed in the O3 ISA exploring both short-term 

exposure related mortality and morbidity have larger (and more statistically 

significant) effect estimates when evaluated for the summer O3 season, relative to the 

full year (see O3 ISA, Figures 6-20 and 6-27). However, if we focus the assessment of 

risk on the warm season, we bias our estimate by excluding potential effects 

associated with cooler (non-summer) months. Given our desire to provide a more 

complete picture of overall risk in each of the study areas, we have favored (for the 

core analysis) effect estimates that cover the full O3 monitoring period specific to 

each study area, rather than the more limited warm (summer) period. 

 Shape of the Functional Form of the Risk Model (including threshold): The O3

ISA concludes that there is little support in the literature for a population threshold for 

short-term O3-attributable effects. However, specifically in relation to mortality, the 

O3 ISA concludes that a national or combined analysis may not be appropriate to 
7-30 

identify whether a threshold exists (see O3 ISA, section 2.5.4.4).22 Given the above 

general observation from the O3 ISA regarding the low potential for thresholds, we 

did not include C-R functions for any of the short-term O3-attributable health 

endpoints modeled that incorporated a threshold.23 To reflect uncertainty about the 

existence and location of a potential threshold in the C-R function for mortality 

attributable to long-term O3 exposures, we include a sensitivity analysis for thresholds 

ranging from 40 to 60 ppb for the summer season average of daily maximum 1-hr O3

concentrations. 

Application of the above criteria resulted in an array of C-R functions specified for the 

risk assessment (see Table 7-2), including functions covering short-term O3-attributable 

mortality and morbidity and long-term O3-attributable mortality. In presenting the C-R functions 

in Table 7-2, we have focused on describing key attributes of each C-R function (and associated 

source epidemiological study) relevant to a review of their use in the risk assessment. More 

detailed technical information including effect estimates and model specification is provided in 

Appendix 7A. Specific summary information provided in Table 7-2 includes: 

 Health endpoints: identifies the specific endpoints evaluated in the study. Generally 

we included all of these in our risk modeling, however, when a subset was modeled, 

we reference that in the “Notes” column (last column in the table). 

 Location: identifies the specific urban areas included in the study and maps those to 

the set of 12 urban study areas included in the risk assessment. 

 Exposure metric: describes the exposure metric used in the study, including the 

specific modeling period (e.g., O3 season, warm season, full year). We developed two 

categories of composite monitor values to match the modeling periods used in the two 

short-term O3-attributable mortality studies providing C-R functions for the analysis. 

For the remaining morbidity endpoints, we mapped specific C-R functions to 

whichever of these two composite monitor categories most closely matched the 

modeling period used in the underlying epidemiological study. This mapping (for 

 

22 Specifically, given the multi-city nature of these mortality studies combined with the variability in O3 and other 

factors related to exposure and risk, the O3 ISA concludes that these studies are not well positioned to evaluate the 

potential for a threshold in the mortality effect. 23 While clinical studies have suggested the presence of a threshold for respiratory effects, these should not be used 

to support specification of population-level thresholds for use in the epidemiological-based risk assessment 

focusing on short-term exposure-related endpoints. The clinical studies focus on relatively small and clearly 

defined populations of healthy adults which are not representative of the broader residential populations typically 

associated with epidemiological studies, including older individuals and individuals with existing health 

conditions which place them at greater risk for O3-related effects. Therefore, the clinical studies are unlikely to 

have the power to capture population thresholds in a broader and more diverse urban residential population, 

should those thresholds exist. 
7-31 

morbidity endpoint C-R functions) is described in the “Notes” column (the seasons 

reflecting in modeling for each C-R function are also presented in Appendix 7A). 

 Additional study design details: this column provides additional information primarily 

covering the lag structure and age ranges used in the study. 

 Application notes: this column provides notes particular to the application of a 

particular epidemiological study and associated C-R functions in the risk assessment. 

7.3.3 Baseline Health Effect Incidence and Prevalence Data 

As discussed earlier (section 7.1.2), the most common epidemiological-based health risk 

model expresses the change in health risk (∆y) associated with a given change in O3 

concentrations (∆x) as a percentage of the baseline incidence (y). To accurately assess the impact 

of O3 air quality on health risk in the selected urban areas, information on the baseline incidence 

of health effects (i.e., the incidence under recent air quality conditions) in each location is 

needed. In some instances, health endpoints are modeled for a population with an existing health 

condition, necessitating the use of a prevalence rate. Where at all possible, we use countyspecific incidences or incidence rates (in combination with county-specific populations). In some 

instances, when county-level incidence rates were not available, BenMAP can employ more 

generalized regional rates (see BenMAP Guidance Manual for additional detail, Abt Associates, 

Inc. 2010). For prevalence rates (which were only necessary for modeling respiratory symptoms 

among asthmatic children using Gent et al. (2008) - see Table 7-2), we utilized a national-level 

prevalence rate appropriate for the age group being modeled. A summary of available baseline 

incidence data for specific categories of effects (and prevalence rates for asthma) is presented 

below: 

 Baseline incidence data on mortality: County-specific (and, if desired, age- and racespecific) baseline incidence data are available for all-cause and cause-specific 

mortality from CDC Wonder.24 The most recent year for which data are available 

online is 2005 and this was the source of incidence data for the risk assessment.25

 Baseline incidence data for hospital admissions and emergency room (ER) visits: 

Cause-specific hospital admissions baseline incidence data are available for each of 

40 states from the State Inpatient Databases (SID). Cause-specific ER visit baseline 

incidence data are available for 26 states from the State Emergency Department 

Databases (SEDD). SID and SEDD are both developed through the Healthcare Cost 

 

24 http://wonder.cdc.gov/mortsql.html 25 Note: For years 1999 – 2005, CDC Wonder uses ICD-10 codes; for years prior to 1999, it uses ICD-9 codes. 

Since most of the studies use ICD-9 codes, this means that EPA will have to create or find a mapping from ICD-9 

codes to ICD-10 codes if the most recent data available are to be used. 
7-32 

and Utilization Project (HCUP), sponsored by the Agency for Healthcare Research 

and Quality (AHRQ). In addition to being able to estimate State-level rates, SID and 

SEDD can also be used to obtain county-level hospital admission and ER visit counts 

by aggregating the discharge records by county. 

 Asthma prevalence rates: state-level prevalence rates that are age group stratified are 

available from the Centers for Disease Control and Prevention (CDC) Behavioral 

Risk Factor Surveillance System (BRFSS) (U.S. CDC, 2010). 

Incidence and prevalence rates are presented as part of the full set of model inputs 

documented in Appendix 7A. The incidence rates and prevalence rates provided in Appendix 7A 

are weighted average values for the age group associated with each of the C-R functions. These 

weighted averages are calculated within BenMAP using more refined age-differentiated 

incidence and prevalence rates originally obtained from the data sources listed in the bullets 

above. 

7.3.4 Population (demographic) Data 

To calculate baseline incidence rates, in addition to the health baseline incidence data we 

also need the corresponding population. We obtained population data from the 2010 U.S. Census 

(http://www.census.gov/popest/counties/asrh/). These data are then used as the basis for backcasting estimates for simulation years (in this case, 2007 and 2009) (see Appendix J of the 

BenMAP User’s Manual for additional detail, U.S. EPA, 2012b). Total population counts used in 

modeling each of the health endpoints evaluated in the analysis (differentiated by urban study 

area and simulation year) are provided as part model inputs presented in Appendix 7A. 

7.4 ADDRESSING VARIABILITY AND UNCERTAINTY 

An important component of a population risk assessment is the characterization of both 

uncertainty and variability. Variability refers to the heterogeneity of a variable of interest within 

a population or across different populations. For example, populations in different regions of the 

country may have different behavior and activity patterns (e.g., air conditioning use, time spent 

indoors) that affect their exposure to ambient O3 and thus the population health response. The 

composition of populations in different regions of the country may vary in ways that can affect 

the population response to exposure to O3 – e.g., two populations exposed to the same levels of 

O3 might respond differently if one population is older than the other. Variability is inherent and 

cannot be reduced through further research. Refinements in the design of a population risk 

assessment are often focused on more completely characterizing variability in key factors 

affecting population risk – e.g., factors affecting population exposure or response – in order to 
7-33 

produce risk estimates whose distribution adequately characterizes the distribution in the 

underlying population(s). 

Uncertainty refers to the lack of knowledge regarding the actual values of inputs to an 

analysis. Models are typically used in analyses, and there is uncertainty about the true values of 

the parameters of the model (parameter uncertainty) – e.g., the value of the coefficient for O3 in a 

C-R function. There is also uncertainty about the extent to which the model is an accurate 

representation of the underlying physical systems or relationships being modeled (model 

uncertainty) – e.g., the shapes of C-R functions. In addition, there may be some uncertainty 

surrounding other inputs to an analysis due to possible measurement error – e.g., the values of 

daily O3 concentrations in a risk assessment location, or the value of the baseline incidence rate 

for a health effect in a population.26 In any risk assessment, uncertainty is, ideally, reduced to the 

maximum extent possible through improved measurement of key variables and ongoing model 

refinement. However, significant uncertainty often remains, and emphasis is then placed on 

characterizing the nature of that uncertainty and its impact on risk estimates. The characterization 

of uncertainty can be both qualitative and, if a sufficient knowledgebase is available, 

quantitative. 

The selection of urban study areas for the O3 risk assessment was designed to cover the 

range of O3-related risk experienced by the U.S. population and, in general, to adequately reflect 

the inherent variability in those factors affecting the public health impact of O3 exposure. 

Sources of variability reflected in the risk assessment design are discussed in section 7.4.1, along 

with a discussion of those sources of variability which are not fully reflected in the risk 

assessment and consequently introduce uncertainty into the analysis. 

The characterization of uncertainty associated with risk assessment is often addressed in 

the regulatory context using a tiered approach in which progressively more sophisticated 

methods are used to evaluate and characterize sources of uncertainty depending on the overall 

complexity of the risk assessment (WHO, 2008). Guidance documents developed by EPA for 

assessing air toxics-related risk and Superfund Site risks (U.S.EPA, 2004 and 2001, respectively) 

as well as recent guidance from the World Health Organization (WHO, 2008) specify multitiered approaches for addressing uncertainty. 

The WHO guidance, in particular, presents a four-tiered approach for characterizing 

uncertainty (see Chapter 3, section 3.2.6 for additional detail on the four tiers included in the 

 

26 It is also important to point out that failure to characterize variability in an input used in modeling can also 

introduce uncertainty into the analysis. This reflects the important link between uncertainty and variability with 

the effort to accurately characterize variability in key model inputs actually reflecting an effort to reduce 

uncertainty about population means and population variability. 
7-34 

WHO’s guidance document). With this four-tiered approach, the WHO framework provides a 

means for systematically linking the characterization of uncertainty to the sophistication of the 

underlying risk assessment. Ultimately, the decision as to which tier of uncertainty 

characterization to include in a risk assessment will depend both on the overall sophistication of 

the risk assessment and the availability of information for characterizing the various sources of 

uncertainty. We used the WHO guidance as a framework for developing the approach used for 

characterizing uncertainty in this risk assessment. 

The overall analysis in the O3 NAAQS risk assessment is relatively complex, thereby 

warranting consideration of a full probabilistic (WHO Tier 3) uncertainty analysis. However, 

limitations in available information prevent this level of analysis from being completed at this 

time. In particular, the incorporation of uncertainty related to key elements of C-R functions 

(e.g., competing lag structures, alternative functional forms, etc.) into a full probabilistic WHO 

Tier 3 analysis would require that probabilities be assigned to each competing specification of a 

given model element (with each probability reflecting a subjective assessment of the probability 

that the given specification is the “correct” description of reality). However, for many model 

elements there is insufficient information on which to base these probabilities. One approach that 

has been taken in such cases is expert elicitation; however, this approach is resource- and timeintensive and consequently, it was not feasible to use this technique in the current O3 NAAQS 

review to support a WHO Tier 3 analysis.27

For most elements of this risk assessment, rather than conducting a full probabilistic 

uncertainty analysis, we have included qualitative discussions of the potential impact of 

uncertainty on risk results (WHO Tier1). As discussed in section 7.1.1, for this risk assessment, 

we have also expanded the sensitivity analysis considerably to cover a range of model elements 

(this represents a WHO Tier 2 analysis). The specific modeling elements covered in the 

sensitivity analysis for each health effects endpoint together with the specification of the core 

analysis is presented in section 7.4.3. As part of the sensitivity analysis, we have also completed 

an influence analysis using estimated elasticities of response28 designed to determine which of 

the input factors used in calculating risk are primarily responsible for inter-city variability in risk. 

This influence analysis focuses on the response of core short-term exposure-related mortality risk 

to inputs since this is one of the key risk metrics completed for the HREA (see section 7.5.3). 

 

27 While a full probabilistic uncertainty analysis was not completed for this risk assessment, we were able to use 

confidence intervals associated with effects estimates (obtained from epidemiological studies) to incorporate 

statistical uncertainty associated with sample size considerations in the presentation of risk estimates. 

28 Elasticities are a measure of sensitivity calculated as the percent change in the response variable for a one percent 

change in the input variable. 
7-35 

In addition to the qualitative and quantitative treatment of uncertainty and variability 

which are described here, we have also completed an analysis to evaluate the representativeness 

of the selected urban study areas against national distributions for key O3 risk-related attributes 

to determine whether they are nationally representative or more focused on a particular portion 

of the distribution for a given attribute (see Chapter 8, section 8.2.1). In addition, we have 

completed a second analysis addressing the representativeness issue, which identified where the 

12 urban study areas included in this risk assessment fall along a distribution of national-level 

short-term and long-term exposure-related mortality risk (see Chapter 8, section 8.2.2). This 

analysis allowed us to assess the degree of which the 12 urban study areas capture locations 

within the U.S. likely to experience elevated levels of risk related to O3 exposure (for both shortterm and long-term O3-attributable mortality). 

The remainder of this section is organized as follows. Key sources of variability which 

are reflected in the design of the risk assessment, along with sources excluded from the design, 

are discussed in section 7.4.1. A qualitative discussion of key sources of uncertainty associated 

with the risk assessment (including the potential direction, magnitude and degree of confidence 

associated with our understanding of the source of uncertainty – the knowledge base) is 

presented in section 7.4.2. The design of the core analysis and sensitivity analysis completed for 

each of the health effect endpoint categories modeled in the risk assessment is discussed in 

section 7.4.3. 

7.4.1 Treatment of Key Sources of Variability 

The risk assessment was designed to cover the key sources of variability related to 

population exposure and exposure response, to the extent supported by available data. Here, the 

term key sources of variability refers to those sources that we believe have the potential to play 

an important role in impacting population risk estimates generated for this risk assessment. 

Specifically, we have concluded that these sources of variability, if fully addressed and 

integrated into the analysis, could result in adjustments to the core risk estimates which might be 

relevant from the standpoint of interpreting the risk estimates in the context of the O3 NAAQS 

review. The identification of sources of variability as “key” reflects consideration for sensitivity 

analyses conducted for previous O3 NAAQS risk assessments (which have provided insights into 

which sources of variability can influence risk estimates) as well as information presented in the 

O3 ISA. 

As with all risk assessments, there are sources of variability which have not been fully 

reflected in the design of the risk assessment and consequently introduce a degree of uncertainty 

into the risk estimates. While different sources of variability were captured in the risk 

assessment, it was generally not possible to separate out the impact of each factor on population 
7-36 

risk estimates, since many of the sources of variability are reflected collectively in a specific 

aspect of the risk model. For example, inclusion of urban study areas from different regions of 

the country likely provides some degree of coverage for a variety of factors associated with O3

risk (e.g., air conditioner use, differences in population commuting and exercise patterns, 

weather). However, the model is not sufficiently precise or disaggregated to allow the individual 

impacts of any one of these sources of variability on the risk estimates to be characterized. 

Key sources of potential variability that are likely to affect population risks are discussed 

below, including the degree to which they are captured in the design of the risk assessment: 

 Heterogeneity in the Effect of O3 on Health Across Different Urban Areas: A 

number of studies cited in the O3 ISA have found evidence for regional heterogeneity 

in the short-term O3-attributable mortality effect (Smith et al., 2009 and Bell and 

Dominici, 2008, Bell et al., 2004, Zanobetti an Schwartz 2008 – see O3 ISA section 

6.6.2.2). These studies have demonstrated that differences in effect estimates between 

cities can be quite substantial (see O3 ISA, Figures 6-32 and 6-33). Therefore, for the 

short-term O3-attributable mortality endpoint modeled using Smith et al., 2009-based 

effect estimates, we have included Bayes-adjusted city-specific effect estimates 

reflecting application of both a regional- and national-prior, both of which are 

intended to capture cross-city differences in effect estimates for the mortality 

endpoint, while still reflecting input from the more stable regional, or national-level 

signal. The national-prior based estimates are included in the core analysis since they 

have greater overall power, while the regional-prior based estimates are included as 

sensitivity analyses to explore the impact of using regional prior in developing the 

Bayes-adjusted estimates (see section 7.4.3).29 For short-term morbidity endpoints, 

typically we have used city-specific effect estimates; however, for most endpoints, we 

only have estimates for a subset of the urban study areas (typically NY, Atlanta 

and/or LA). Therefore, although our risk estimates do reflect the application of cityspecific effect estimates, because we do not have estimates for all 12 urban study 

areas, we do not provide comprehensive coverage for heterogeneity in modeling the 

respiratory morbidity endpoint category. Long-term O3-attributable mortality has 

been shown to demonstrate regional heterogeneity. Specifically, Jerrett et al. (2009) 

presented regional effect estimates that demonstrated considerable heterogeneity 

ranging from essentially a no-effect (for the Northeast and Industrial Midwest) to 

effects substantially larger than the national effect (Southeast, Southwest and Upper 

 

29 Note, that in some instances, there may be insufficient variance between cities to generate city-specific estimates 

using a regional prior, which compromises their use in the core analysis. 
7-37 

Midwest) (see Table 4 in Jerrett et al., 2009). There are many potential explanations 

for regional heterogeneity including differences in O3-attributable factors and 

potential confounding, potential for the presence of (and regional differences in) 

averting behavior, and variation in sample sizes which can impact stability of effect 

estimates. For the core analysis, we use a national effect estimate in modeling longterm exposure related mortality. Consideration of regional effect estimates are 

included as a sensitivity analysis (see section 7.4.3 and 7.5.3). 

 Exposure Measurement Error Associated with O3 Effect Estimates: Exposure 

measurement error refers to uncertainty associated with using ambient monitor based 

exposure surrogate metrics to represent the actual exposure of an individual or 

population. As such, this factor can be an important contributor to variability in 

epidemiological study results across locations, and uncertainty in results for any 

specific city (O3 ISA, p. 1xii). Exposure measurement error can result from a number 

of factors (e.g., central site monitors not representing actual patterns of personal 

exposure including activity patterns, presence of non-ambient sources of exposure for 

the pollutant of interest) (O3 ISA, 1xii). These factors can vary across urban study 

areas (and even within urban study areas), thereby contributing to differences in the 

nature and magnitude of exposure measurement error across locations and ultimately 

to differences in effect estimates and associated confidence levels. Exposure 

measurement error is related to heterogeneity in effect estimates, since regional 

differences in effect estimates can result in part, from differences in exposure 

measurement error as noted here. 

 Intra-urban Variability in Ambient O3 Levels: The picture with regard to within 

city variability in ambient O3 levels and the potential impact on epidemiologic-based 

effect estimates is somewhat more complicated. The O3 ISA notes that spatial 

variability in O3 levels is dependent on spatial scale with O3 levels being more 

homogeneous over a few kilometers due to the secondary formation nature of O3, 

while levels can vary substantially over tens of kilometers. Community exposure may 

not be well represented when monitors cover large areas with several subcommunities having different sources and topographies as exemplified by Los 

Angeles which displays significantly greater variation in inter-monitor correlations 

than does, for example, Atlanta or Boston (see O3 ISA, section 4.6.2.1). Despite the 

potential for substantial variability across monitors the O3 ISA notes that studies have 

tended to demonstrate that monitor selection has only a limited effect on the 

association of short-term O3 exposure with health effects. The likely explanation for 

this is that, while absolute values for a fixed point in time can vary across monitors in 
7-38 

an urban area, the temporal patterns of O3 variability across those same monitors 

tends to be well correlated. Given that most of the short-term O3-attributable O3

epidemiological studies are time series in nature, the O3 ISA notes that the stability of 

temporal profiles across monitors within most urban areas means that monitor 

selection will have little effect on the outcomes of an epidemiological study 

examining short-term O3-attributable mortality or morbidity (see O3 ISA, section 

4.6.2.1). For this reason, we conclude that generally intra-city heterogeneity in O3

levels is not a significant factor likely to impact estimates of short-term O3-

attributable risk. One exception is LA which, due to its size and variation in O3

sources and other factors impacting O3 patterns such as topography, displays 

significant variation in ambient O3 levels with a subsequent impact on risk. However, 

in the case of LA (as with the other urban study areas), we model risk using 

composite monitors which do not provide spatially-differentiated representations of 

exposure and consequently, we do not address this source of variability in the risk 

assessment. As discussed in the uncertainty section, short-term exposure mortality 

effect estimates for the New York CBSA (Smith et al., 2009) display significant 

variability. However, it is not clear which factors are primarily responsible for this 

heterogeneity (e.g., differences in the urban structure, residential behavior, or ambient 

O3 levels within the CBSA). The potential for intra-city heterogeneity in O3 levels to 

affect risk is more pronounced with long-term O3-attributable mortality where the 

relationship between annual trends in ambient O3 (as represented using composite 

monitor values) and annual mortality is compared between urban study areas in order 

to derive effect estimates. Here, pronounced heterogeneity in O3 levels within a given 

city can result in exposure misclassification, if that heterogeneity is not well 

represented by the composite monitor for that city. Different degrees of exposure 

misclassification across urban study areas can introduce uncertainty into the overall 

national-level effect estimate for long-term exposure-related mortality. Furthermore, 

if that exposure measurement error has a regional trend, then measurement error can 

potentially result in apparent regional heterogeneity in the effect estimates. The 

degree to which there is true regional heterogeneity is made uncertain by the presence 

of differential measurement error across regions. 

 Variability in the Patterns of Ambient O3 Reduction across Urban Areas: The 

simulated patterns of ambient O3 concentrations across an urban area can vary based 

on the methodology used to adjust ambient O3 concentrations to represent just 

meeting the existing or alternative suites of standards. For the 1st draft HREA, we 

used a statistical approach called the “quadratic rollback” method for simulating just 
7-39 

meeting the existing O3 standard. Although the quadratic rollback method replicates 

historical patterns of air quality changes better than some alternative methods, its 

implementation relies on a statistical relationship instead of on a mechanistic 

characterization of physical and chemical processes in the atmosphere. Because of its 

construct as a statistical fit to measured O3 values, the quadratic rollback technique 

cannot capture spatial and temporal heterogeneity in O3 response and also cannot 

account for nonlinear atmospheric chemistry that causes increases in O3 as a result of 

emissions reductions of certain O3 precursors under some circumstances. As noted in 

section 7.1.1, for this HREA, we have employed a model-based O3 adjustment 

methodology in the risk assessment for simulating O3 concentrations under existing 

and alternate standard levels. Use of this model-based approach allows the risk 

assessment results to more fully account for non-linearities in O3 formation and to 

reflect spatial and temporal heterogeneity in O3 response, including NOx titration 

conditions under which a reduction in NOx causes an increase in O3 concentrations, in 

some core urban locations. 

 Demographics and Socioeconomic-status (SES)-related Factors: Variability in 

population density, particularly in relation to elevated levels of O3 has the potential to 

influence population risk, although the significance of this factor also depends on the 

degree of intra-urban variation in O3 levels (as discussed above). In addition, 

community characteristics such as pre-existing health status, ethnic composition, SES 

and the age of housing stock (which can influence rates of air conditioner use thereby 

impacting rates of infiltration of O3 indoors) can contribute to observed differences in 

O3-related risk (see O3 ISA, section 2.5.4.5). Some of the heterogeneity observed in 

effect estimates between cities in the multicity studies may be due to these 

community characteristics, and while we cannot determine how much of that 

heterogeneity is attributable to these factors, the degree of variability in effect 

estimates between cities in our analysis should help to capture some of the latent 

variability in these community characteristics. 

 Baseline Incidence of Disease: We collected baseline health effects incidence data 

(for mortality and morbidity endpoints) from a number of different sources (see 

section 7.3.3). Often the data were available at the county-level, providing a relatively 

high degree of spatial refinement in characterizing baseline incidence given the 

overall level of spatial refinement reflected in the risk assessment as a whole. 

Otherwise, for urban study areas without county-level data, either (a) a surrogate 

urban study area (with its baseline incidence rates) was used, or (b) less refined statelevel or national incidence rate data were used. 
7-40 

7.4.2 Qualitative Assessment of Uncertainty 

As noted in section 7.4, we have based the design of the uncertainty analysis carried out 

for this risk assessment on the framework outlined in the WHO guidance document (WHO, 

2008). That guidance calls for the completion of a Tier 1 qualitative uncertainty analysis, 

provided the initial Tier 0 screening analysis suggests there is concern that uncertainty associated 

with the analysis is sufficient to significantly impact risk results (i.e., to potentially affect 

decision making based on those risk results). Given previous sensitivity analyses completed for 

prior O3 NAAQS reviews, which have shown various sources of uncertainty to have a potentially 

significant impact on risk results, we believe that there is justification for conducting a Tier 1 

analysis. 

For the qualitative uncertainty analysis, we have described each key source of uncertainty 

and qualitatively assessed its potential impact (including both the magnitude and direction of the 

impact) on risk results, as specified in the WHO guidance. Similar to our discussion of 

variability in the last section, the term key sources of uncertainty refers to those sources that the 

we believe have the potential to play an important role in impacting population incidence 

estimates generated for this risk assessment (i.e., these sources of uncertainty, if fully addressed 

could result in adjustments to the core risk estimates which might impact the interpretation of 

those risk estimates in the context of the O3 NAAQS review). These key sources of uncertainty 

have been identified through consideration for sensitivity analyses conducted for previous O3

NAAQS risk assessments, together with information provided in the final O3 ISA and comments 

provided by CASAC on the analytical plan for the risk assessment. 

Table 7-4 includes the key sources of uncertainty identified for the epidemiological-based 

risk portion of the O3 HREA. For each source of uncertainty, we have (a) provided a description, 

(b) estimated the direction of influence (over, under, both, or unknown) and magnitude (low, 

medium, high) of the potential impact of each source of uncertainty on the risk estimates, (c) 

assessed the degree of uncertainty (low, medium, or high) associated with the knowledge-base 

(i.e., assessed how well we understand each source of uncertainty), and (d) provided comments 

further clarifying the qualitative assessment presented. 

The categories used in describing the potential magnitude of impact for specific sources 

of uncertainty on risk estimates (i.e., low, medium, or high) reflect our consensus on the degree 

to which a particular source could produce a sufficient impact on risk estimates to influence the 

interpretation of those estimates in the context of the O3 NAAQS review.30 Sources classified as 

 

30 For example, if a particular source of uncertainty were more fully characterized (or if that source was resolved, 

potentially reducing bias in a core risk estimate), could the estimate of incremental risk reduction in going from 
7-41 

having a “low” impact would not be expected to impact the interpretation of risk estimates in the 

context of the O3 NAAQS review; sources classified as having a “medium” impact have the 

potential to change the interpretation; and sources classified as “high” are likely to influence the 

interpretation of risk in the context of the O3 NAAQS review. Because this classification of the 

potential magnitude of impact of sources of uncertainty is not based on our direct quantitative 

assessments, we use qualitative judgments, in some cases informed by other relevant quantitative 

analyses. Therefore, the results of the qualitative analysis of uncertainty are not useful for 

making quantitative estimates of confidence, e.g. probabilistic statements about risk. However, 

they can be used to support the interpretation of the risk estimates, including the assessment of 

overall confidence in the risk estimates. In addition, they can also be used in guiding future 

research to reduce uncertainty related to O3 risk assessment. As with the qualitative discussion of 

sources of variability included in the last section, the characterization and relative ranking of 

sources of uncertainty addressed here is based on our consideration of information provided in 

previous O3 NAAQS risk assessments (particularly past sensitivity analyses), the results of risk 

modeling completed for the current O3 NAAQS risk assessment and information provided in the 

O3 ISA as well as earlier O3 Criteria Documents. Where appropriate, in Table 7-4, we have 

included references to specific sources of information considered in arriving at a ranking and 

classification for a particular source of uncertainty. 

 

the current to an alternative standard level change sufficiently to produce a different conclusion regarding the 

magnitude of that risk reduction in the context of the O3 NAAQS review? 
7-42 

Table 7-4. Summary of Qualitative Uncertainty Analysis of Key Modeling Elements in the O3 NAAQS Ris

Source Description 

Potential Influence of 

Uncertainty on Risk 

Estimates 

KnowledgeBase 

Uncertainty* 

Comme

Direction Magnitude (KB: knowledge base, INF: influence 

A. Adjustment of recent air quality measurements of O3 to simulate just meeting 

the existing and alternative standard levels 

See Chapter 4 for details Both Low- Medium Low-medium See Chapter 4 for more details 

B. Use of CBSA-based study areas in modeling risk (i.e., potential mismatch between study areas used in the HREA and study areas used in the epidemiological studies providing the effect estimates used in modeling health effect endpoints) 

If the set of monitors used in a particular urban study area to characterize population exposure as part of an ongoing risk assessment do not match the ambient monitoring data used in the original epidemiological study, then uncertainty can be introduced into the risk estimates. This uncertainty is balanced in part by the reduction in bias that results from using the expanded CBSA definition. (See section 7.1.1 for more details.) However, it should be noted that because these epidemiological studies occurred in the past, sometimes it can be impossible to exactly match the monitors used in the study using recent air quality data given that monitors may have moved to a different location or there may not be measurements available at specific monitors in the 

more recent time period. 

Both Low- medium Low-medium 

KB and INF: In modeling risk for the HRareas for all health effect endpoints. As of the larger CBSA study areas allows uin air quality affects risk across the entirintroducing known bias into the HREA bsubpopulation living in areas likely to ex

(and excluding the larger population of experience reductions in ambient O3 lev

CBSA-based study areas addresses thintroduces uncertainty into the REA sincHREA study areas to the study areas in providing the effect estimates used in mGiven available data, it is not possible athe degree of uncertainty introduced intmismatch in study areas. However, the use of the larger CBSA study areas (witsubstantial, as illustrated in the sensitivarea (see section 7.5.3). 

C. Application of C-R functions based on a specific temporal and spatial pattern of correlations between O3

monitors in an urban area (as reflected in the epidemiological study providing the effect estimates) to a simulated change in the patterns of those correlations when we estimate risk in the HREA. 

The effect estimates used in this risk assessment reflect a specific spatial and temporal pattern of ambient O3 (as 

represented by the particular monitoring network providing data for the underlying epidemiological study). However, if the spatial and temporal pattern of O3 levels in the study areas 

being modeled differ significantly from the patterns in the original epidemiological study (for those same study areas), then uncertainty can be introduced into the risk estimates. 

Both Low- medium Low-medium 

KB and INF: With application of the HDsimulate potential changes in the spatia

study areas when just meeting the existrelative to patterns under recent conditithe application of the original effect estisurrogate represented by the composite match that of the underlying epidemiolopossible, given available data, to characof this uncertainty. This is probably mosYork and Los Angeles where simulation alternative standards using the HDDM-aNOx reductions and there is very little da

O3 concentrations. 

D. Characterizing intraurban population exposure in the context of 

Exposure misclassification within communities that is associated with the use of generalized population monitors 

Under 

(generally) 

Lowmedium Medium KB and INF: Despite the potential for su

across monitors (particularly in larger ursources and topography such as L.A.), 
7-43 

Source Description 

Potential Influence of 

Uncertainty on Risk 

Estimates 

KnowledgeBase 

Uncertainty* 

Comme

Direction Magnitude (KB: knowledge base, INF: influence 

epidemiology studies linking O3 to specific health 

effects 

(which may miss important patterns of exposure within urban study areas) introduces uncertainty into the effect estimates obtained from epidemiology studies. 

tended to demonstrate that monitor selethe association of short-term O3 exposu

section 4.6.2.1). However, this issue courban areas which may exhibit greater v

sources, topography and patterns of copotential for population living in the vicinexperience different patterns of exposuurban populations (both for O3 and co-p

E. Statistical fit of the C-R functions 

Exposure measurement error combined with other factors (e.g., size of the effect itself, sample size, control for confounders) can affect the overall level of confidence associated with the fitting of statistical effect-response models in epidemiological studies. 

Both 

Medium (short-term health endpoints) 

Medium 

INF: For short-term mortality and morbigreater uncertainty associated with the sample sizes often involved, difficulty in time period for short-term O3 exposure, 

fitted to individual counties or urban arefor varying degrees of confounding and locations). These studies can also have statistically significant. For this risk assemortality, we are not relying on locationusing city-specific effects estimates der(these combine national-scale models wmeasurement error (uncertainty associato represent exposure of an individual oimportant contributor to uncertainty in eshort-term and long-term O3-attributable 

with other factors (e.g., low data densityresult in the smoothing of epidemiologicthe obscuring of thresholds should they 

exposure measurement error can vary awithin the same urban study area. For ehave an activity pattern that results in cstudy area) being particularly poor at reambient O3. In this example, an effect e

population based on O3 exposure chara

would have increased uncertainty relativother population with different activity pmeasurement error. (for long-term expodiscussion of overall confidence in sect

F. Shape of the C-R functions 

Uncertainty in predicting the shape of the C-R function, particularly in the lower exposure regions which are often the focus in O3 NAAQS reviews. 

Both Medium Low-medium 

KB and INF: Studies reviewed in the O3 

shape of the O3 C-R curve for short-term 

with possible “thresholds” (i.e., O3 conc

in order to elicit an observable health relinear C-R function with no indication of examined 8-h max and 24-h avg O3 con

notes that the studies from which the Cthere is less certainty in the shape of thdistribution of O3 concentrations (in the 

density of data in the studies in this ran
7-44 

Source Description 

Potential Influence of 

Uncertainty on Risk 

Estimates 

KnowledgeBase 

Uncertainty* 

Comme

Direction Magnitude (KB: knowledge base, INF: influence 

existence and location of a potential thrmortality attributable to long-term O3 ex

analysis for thresholds ranging from 40 average of daily maximum 1-hr O3 conc

G. Addressing copollutants 

The inclusion or exclusion of copollutants which may confound, or in other ways, affect the O3 effect, 

introduces uncertainty into the analysis. 

Both Low- medium Medium 

KB and INF: The O3 ISA notes that acro

PM indices on O3-mortality risk estimate

the variation in O3-mortality risk estimat

O3 effects are independent of the relatio

However, interpretation of the potential 

mortality risk estimates requires caution

correlation varies across regions, due to complicating the interpretation of the corelationship between O3 and mortality. A

component datasets used as a result of sampling schedule instituted in most citsample size employed to examine whetconfounds the O3-mortality relationship 

H. Specifying lag structure (short-term exposure studies) 

There is uncertainty associated with specifying the exact lag structure to use in modeling short-term O3-attributable mortality and respiratory-related morbidity. 

Both Low- Medium Low 

KB and INF: The majority of studies exathat O3 effects on mortality occur within 

studies examining the impact of O3 exp

morbidity endpoints suggests a rather imfew days of O3 exposure (see O3 ISA, s

the exact nature of the ideal lag models are fairly confident that they would be ofollowing exposure. 

I. Using studies from one geographic area to cover urban areas outside of the study area 

In the case of Gent et al., 2003 (used in modeling asthma exacerbations in Boston), we are using C-R functions based on an epidemiological study of a region (northern Connecticut and Springfield) that does not encompass the actual urban study area assessed for risk (Boston). 

Both Medium Low 

INF: Factors related to O3 exposure incl

levels etc may differ between the region study and Boston. If these differences aestimate from the epidemiological study considerable uncertainty and potential b

J. Characterizing baseline incidence rates 

Uncertainty can be introduced into the characterization of baseline incidence in a number of different ways (e.g., error in reporting incidence for specific endpoints, mismatch between the spatial scale in which the baseline data were captured and the level of the risk assessment). 

Both Low- medium Low 

INF: The degree of influence of this souestimates likely varies with the health econsideration. There is no reason to bebiases in estimates of the baseline incidestimates that are expressed as incremalternative standards should be relativeuncertainty. KB: The county level baseline incidence county level were obtained from data bauncertainty is low. 

* Refers to the degree of uncertainty associated with our understanding of the phenomenon, in the context of assessing and characterizi(specifically in the context of modeling PM risk).
7-45 

7.4.3 Description of Core and Sensitivity Analyses 

As discussed in section 7.1.1, this risk assessment includes a set of core (higher 

confidence) risk estimates which are supplemented by sensitivity analyses. The sensitivity 

analyses explore the potential impact that variation in specific model design elements can have 

on the core risk estimates. This section specifies which design elements are included in both the 

core and sensitivity analyses completed for each of the health effect endpoint categories included 

in the risk assessment. We divided the sensitivity analyses into two categories: (a) those 

involving air quality characterization and (b) those associated directly with the specification of 

the C-R functions used in estimating risk. We recognize that there can be overlap between these 

categories with some modeling elements (e.g., modeling period) affecting both the composite 

monitor distribution as well as representing an element of C-R function specification. However, 

we have retained these two categories to aid in the presentation and discussion of sensitivity 

analysis results.31 The sensitivity analyses also included an initial influence analysis designed to 

evaluate which of the model inputs are primarily responsible for inter-city variability 

(heterogeneity) in risk. The influence analysis uses estimated elasticities of risk with respect to 

the risk function input variables, focusing on the short-term exposure-related mortality endpoint 

and associated input parameters since this is one of the key risk estimates generated for the 

HREA (additional detail on how the influence analysis was conducted is presented in section 

7.5.3). 

Table 7-5 presents the alternative approaches for adjusting the O3 distributions used in 

the sensitivity analysis and also identifies the approaches used in the core analysis for each of the 

study areas. The alternative air quality adjustment approaches examine the differences in 

changes in air quality and risk when applying NOx-only versus NOx and VOC reductions in the 

HDDM-adjustment approach. It should be noted that when NOx and VOC reductions were used 

in the HDDM-adjustment approach in this sensitivity analysis, the same percent reduction for 

both pollutants was used in the air quality adjustment for meeting the existing and alternative 

standard in each urban area. More details on these alternative air quality adjustment approaches 

are discussed in Chapter 4 and appendices. 

 

31 In presenting both the core and sensitivity analyses, we include both point estimates and 95th percentile confidence 

interval (CI), with the latter reflecting the statistical fit of the effect estimates (and hence the power of the 

underlying epidemiological study). In comparing core and sensitivity analyses, we not only focus on point 

estimates, but also on the CIs since they provide insights into differences in the degree of statistical support for the 

effect estimates underlying the risk estimates and therefore, overall confidence in those estimates. 
7-46 

Besides the approach used to adjust the distributions of O3, another fact which has a 

direct impact on composite monitor composition is the specification of the study area (since this 

determines the mix of monitors that will be included in constructing the composite monitor). As 

discussed in section 7.1.1, for the core analysis, we modeled all endpoints (for all study areas) 

using CBSA-based study areas. For the sensitivity analysis (for the short-term O3-attributable 

mortality endpoint), we included a smaller study area based on the original study area definition 

used in the Smith et al., 2009 study.32

Table 7-6 presents the model elements included in sensitivity analyses exploring 

alternative C-R function specifications. These sensitivity analyses were applied both to shortterm O3-attributable mortality and long-term O3-attributable mortality. As discussed in section 

7.1.1, we were not able to differentiate between alternative C-R function specifications for shortterm O3-attributable morbidity endpoints and therefore included the full set of alternative C-R 

function specifications in the core analysis. This results in a distribution of core risk estimates for 

each endpoint which can be used to gain insights into the impact of different C-R function 

specifications on risk. Because separate sensitivity analyses were not completed for short-term 

O3-attributable morbidity endpoints, this category is not included in Table 7-6. 

 

 

32 We did not include an alternative study area simulation as a sensitivity analysis for long-term exposure related 

mortality since, for the core analysis, we are using a single (national) effect estimate in modeling this endpoint, 

and consequently, the use of an effect estimate from a smaller study area to represent a somewhat larger area (as is 

the case with short-term O3-attributable mortality) is likely to introduce less uncertainty. 
7-47 

Table 7-5. Specification of the Core and Sensitivity Analyses (air quality simulation). 

Study Area

Core Simulation 

(type of precursor reduced to 

adjust O3 distribution) Sensitivity Analysis

Atlanta, GA NOx-only 

Alternative modeling 

approach not evaluated 

Baltimore, MD NOx-only 

Boston, MA NOx-only 

Cleveland, OH NOx-only 

Denver, CO NOx & VOC NOx-only 

Detroit, MI NOx-only NOx & VOC 

Houston, TX NOx-only NOx & VOC 

Los Angeles, CA NOx-lower bound* NOx & VOC-lower bound* 

New York, NY NOx-lower bound* (exclude 60) NOx & VOC-lower bound* 

Philadelphia, PA NOx-only NOx & VOC 

Sacramento, CA NOx-only NOx & VOC 

St. Louis, MO NOx-only Alternative modeling 

approach not evaluated 

A lower-bound fit of the HDDM-based O3 sensitivities (reflecting a greater increment of O3 reduction per 

unit of VOC and/or NOx reduction) was required in simulation of the alternative standard levels.

Table 7-6. Specification of the Core and Sensitivity Analyses (alternative C-R function 

specification). 

Health Effect 

Endpoint 

Category 

Modeling Elements Included 

Core Analysis Sensitivity Analysis 

Short-term 

O3-

attributable 

mortality 

- Full monitoring period 

(specific to each study area), 

8-hr max metric, nationalBayes adjusted, single 

pollutant model. 

 - effect estimates obtained 

from: Smith et al. (2009) 

- summer (warm month), 8-hr mean, regional-Bayes 

adjusted, multi-pollutant (with PM10). 

- effect estimates obtained from Zanobetti and Schwartz 

(2008) and Smith et al. (2009) 

Long-term 

O3-

attributable 

mortality 

- Single national estimate, 

two-pollutant model (PM2.5), 

long-term peak trend metric 

(based on daily 1-hr max 

values), CBSA-based study 

area. 

- effect estimates obtained 

from Jerrett et al. (2009) 

study 

- Regional-differentiated effect estimates, single pollutant 

model. 

- National-level effect estimate, single pollutant model. 

- Effect estimates reflecting consideration for potential 

thresholds in the respiratory mortality effect (ranging from 

40 to 60 ppb) 

- All effect estimates for this sensitivity analysis were also 

obtained from Jerrett et al., 2009 study (with the exception 

of the threshold models – which were obtained through 

direct communication with the authors; Sasser, 2014) 
7-48 

7.5 URBAN STUDY AREA RESULTS 

This section discusses risk estimates generated for the set of 12 urban study areas, 

including both the core risk estimates and accompanying sensitivity analyses. In summarizing 

risk estimates, this discussion focuses on results most relevant to two policy-related questions: 

(a) to what extent is the existing O3 standard protective of public health and, (b) what is the 

nature and magnitude of additional public health protection provided by the suite of alternative 

standards under consideration? Consequently, we focus on two types of risk estimates including 

the magnitude of O3-attributable risk after simulation of just meeting the existing standard and 

the degree of risk reduction potentially provided by each of the alternative standards relative to 

just meeting the existing standard.33

This section is organized as follows. We begin by presenting the core risk estimates in 

both tabular and graphical format at the end of this section. We then present key observations 

about the risk estimates for just meeting the existing standard (for core risk) in section 7.5.1. Key 

observations related to risk estimates for just meeting alternative standard levels, and for 

estimates of risk changes comparing alternative standards to just meeting the existing standard 

(again, for core risk) are presented in section 7.5.2. After presenting key observations related to 

the core risk estimates, we then present key observations resulting from the sensitivity analyses 

(section 7.5.3). 

A number of details regarding the design of the core risk assessment should be kept in 

mind when reviewing the core risk estimates presented in this section (see section 7.1.1 for 

additional detail on these design elements): 

 All risk estimates reflect application of a CBSA-based study area. 

 Estimates are presented for two simulation years (2007 and 2009) 

 Short-term O3-attributable mortality estimates are generated for all 12 urban study 

areas, while most short-term O3-attributable morbidity estimates (depending on the 

specific health endpoint) are generated for only a subset of urban study areas. Longterm O3-attributable mortality is modeled for all 12 urban study areas. 

 For all health effect endpoints, we model risk down to zero O3 and do not include 

either consideration for LML or alternative threshold levels. 

There are several categories of risk metrics generated for the core mortality and 

morbidity endpoints modeled in this analysis. Below we describe both the types of risk metrics 

 

33 As part of this HREA, we have also generated estimates of risk under recent conditions as well as estimates of the 

degree of risk reduction (relative to risk under recent conditions) associated with adjusting air quality to just meets 

the existing standard. See Appendix 7B. 
7-49 

generated for the core analysis and the specific types of tables and figures used in presenting 

those metrics. 

I. Core short-term O3-attributable mortality estimates 

 Table presenting estimates of O3-attributable mortality risk after just meeting 

the existing standard and the estimated change in mortality associated with 

meeting each of the alternative standard levels relative to the existing standard 

(Table 7-7): These estimates include point estimates and 95th percentile confidence 

intervals representing uncertainty associated with the statistical fit of the effect 

estimates. 

 Table presenting estimates of the percent of total mortality attributable to O3

after just meeting the existing standard and the percent reduction in O3-

attributable risk associated with each alternative standard (Table 7-8).

 Heat maps for mortality illustrating distribution across daily O3 levels of total 

O3-attributable risk after just meeting the existing standard and risk reductions 

after meeting alternative standards (Figure 7-2 and Figure 7-3): Heat maps are 

provided for each of the 12 urban areas. The color gradient in each figure reflects the 

distribution of mortality (or the change in mortality) across the range of daily 8-hr O3

levels and provides a visual tool to explore trends in mortality counts across daily O3

levels and between urban study areas. Visual patterns in the figures presenting total 

risk and risk reduction are interpreted differently: 

o For figures depicting total O3-attributable risk, colors range from blue (lower 

mortality count) to red (higher mortality count). As an example, with Figure 7-2, 

top heat map (which presents total O3-attributable risk for the existing standard in 

2007, based on Smith et al., 2009 C-R functions), if we focus on the first row 

(Atlanta, GA), we see a value of 31 under the column 55-60 ppb. This value 

reflects the fact that 31 of the 270 O3-attributable deaths estimated for Atlanta 

after just meeting the existing 75 ppb standard in 2007 occurred on days with 

composite monitor O3 levels between 55 and 60 ppb. Similarly, in the same row, 

we see that only two O3 attributable deaths occurred on days when the composite 

monitor value was between 20 and 25 ppb. We also include the total O3-

attributable mortality (for each study area) in the final column marked “Total”. 
7-50 

o For figures depicting changes in risk associated with simulation of existing and 

alternative standard levels, we see that the pattern is more complex since we can 

have a combination of increases and decreases in risk in the heat maps, with 

increases in risk identified as red to yellow and decreases in risk identified as 

yellow to blue. Increases in risk are negative numbers, decreases are positive. In 

addition, in the final three columns of each map, we provide estimates of the total 

O3-attributable mortality, as well as the total broken down into the subtotals 

across days with increases (negative) and days with decreases (positive) in that 

mortality. The increase and decrease for a given study area should sum 

(accounting for rounding in these subtotals) to the overall total for O3-attributable 

deaths for that study area.34 Several factors can contribute to the patterns of 

changes in O3-attributable risk reflected in these maps. For example, nonlinearities in O3 formation can result in increases in O3 on some days, even when 

simulating air quality just meeting a lower alternative standard (see section 7.1.1). 

In addition, simulation of alternative standard levels can result in a change in the 

overall distribution of the composite monitor ambient O3 distribution. Often, this 

change will take the form of a shift in the upper tail of the distribution towards the 

mean, given that simulated air quality just meeting alternative standard levels 

targets higher O3 days. If we look at Figure 7-2 at the second map (Decrease 75 to 

70) and specifically at the row for Houston, we see that there is a -3 increase in 

deaths distributed across 20-35 ppb days and a decrease in deaths of 8, primarily 

distributed across 40-60 ppb days. 

 Graphic plots of O3-attributable deaths per 100,000 population for just meeting 

the existing and alternative standards (Figure 7-4): This plot provides estimates 

that are adjusted for the size of the underlying urban population, thereby allowing the 

mortality estimates and associated trends to be more readily compared across urban 

study areas (consideration of absolute O3 mortality is complicated by the role that 

underlying urban population plays in driving total O3-attributable mortality – larger 

study areas like Los Angeles and New York having substantially larger mortality 

estimates primarily due to their higher underlying populations). These figures allow 

us to evaluate the overall magnitude of risk reductions across standard levels and 

determine the degree to which those trends differ for different study areas.

 

34 The “Change in Risk” totals at the right edge of each heat map may not sum exactly to the total (for a given row) 

due to rounding. 
7-51 

Tables summarizing O3-attributable morbidity counts, percent of baseline incidence and 

percent reduction in O3-attributable risk for short-term O3-attributable morbidity (Table 7-9 

through Table 7-11): Three categories of short-term O3-attributable morbidity effects were 

modeled for the analysis (respiratory related HA, respiratory-related ER visits and asthma 

exacerbations). As discussed in section 7.1.1, these morbidity effects were modeled for a 

combination of all 12 urban study areas and a subset of those study areas depending on the 

endpoint (see below). The C-R functions available for modeling many of these morbidity 

endpoints included consideration for a number of design elements (e.g., co-pollutants and lag 

structure). However, as noted earlier in section 7.1.1, for short-term exposure morbidity 

endpoints with multiple C-R functions, we were not able to differentiate between C-R functions 

in terms of overall confidence and consequently we could not identify a single core model. 

Therefore, when we have multiple C-R functions reflecting different treatments of key design 

elements such as lag structure, we consider the risk estimates that result from the full set of C-R 

functions to represent a core range of risk. Each of the tables summarizing short-term O3-

attributable morbidity risk present several risk metrics including: (a) total O3-attributable counts 

(after just meeting the existing standard), (b) reductions in O3-attributable counts (for each of the 

alternative standard levels relative to just meeting the existing standard), (c) percent of baseline 

incidence attributable to O3 (after just meeting the existing standard) and (d) percent reductions 

in O3-attributable risk (for each of the alternative standard levels). In presenting these morbidity 

risk estimates, we do not include 95th percentile confidence intervals (CIs) in order to conserve 

space (CIs are included in the detailed tables in Appendix 7B). Specific tables summarizing these 

morbidity risk estimates include: 

o HA visits (for respiratory symptoms including asthma): Table 7-9 presents 

estimates of HA (for respiratory symptoms, chronic lung disease and asthma). 

Risk estimates are generated for a subset of the urban study areas for some of the 

health endpoints (e.g., New York City for HA [chronic lung disease and asthma]), 

while HA (respiratory-related) estimates cover all 12 urban study areas. 

o ER visits (for respiratory symptoms including asthma): Table 7-10 presents 

estimates of ER visits (for respiratory symptoms and asthma) specifically for New 

York City and Atlanta based on C-R functions obtained from several 

epidemiological studies. 

o Asthma exacerbations: Table 7-11 presents estimates of asthma exacerbations 

(including estimates for a range of symptoms) for Boston, the only urban study 

area with C-R functions supporting modeling for this endpoint. 
7-52 

 Graphic plots of O3-attributable respiratory-related HA per 100,000 residents 

for the existing and alternative standard levels (Figure 7-5): This figure is 

intended to complement Figure 7-4 which presents the same type of risk information 

for short-term O3-attributable mortality. By plotting respiratory HA per 100,000, we 

adjust for the underlying population which makes trends in risk more comparable 

across urban study areas. We have only created this graphic for respiratory HA (based 

on application of Medina-Ramon et al., 2006) since that is the only morbidity 

endpoint modeled for all 12 urban study areas. As with the mortality figure, this 

figure allows us to evaluate the overall magnitude of risk reductions across standard 

levels and determine the degree to which those trends differ for different study areas. 

III. Core long-term O3-attributable mortality estimates 

 Table presenting estimates of long-term O3-attributable mortality including total 

risk after just meeting the existing standard and risk reductions based on 

comparing risks after meeting alternative standards to risks after meeting the 

existing standard (Table 7-12): Estimates presented in Table 7-12 reflect respiratory 

mortality and include 95th percentile confidence intervals representing uncertainty 

associated with the statistical fit of the effect estimates used. Estimates presented in 

these tables allow for consideration for the magnitude of risk associated with just 

meeting the existing standard and the pattern of risk reduction in meeting alternative 

standards relative to the existing standard. 

 Table presenting estimates of the percent of respiratory mortality attributable to 

O3 and percent reductions in O3-attributable risk for long-term O3-attributable 

mortality (Table 7-13).

Graphic plots of O3-attributable deaths per 100,000 population for just meeting the 

existing and alternative standards (Figure 7-6): This plot provides estimates that are adjusted 

for the size of the underlying urban population, thereby allowing the mortality estimates and 

associated trends to be more readily compared across urban study areas (consideration of 

absolute O3 mortality is complicated by the role that underlying urban population plays in 

driving total O3-attributable mortality – larger study areas like Los Angeles and New York 

having substantially larger mortality estimates primarily due to their higher underlying 

populations). As with similar plots for short-term exposure-related mortality and morbidity, these 

figures allow us to evaluate the overall magnitude of risk reductions across standard levels and 

determine the degree to which those trends differ for different study areas. 
7-53 

Table 7-7. Short-Term O3-attributable All-Cause Mortality, 2007 and 2009 Air Quality. 

Smith et al. (2009) C-R Functions, O3 season, CBSA-based study area, no threshold. 

NA: for NY, the model-based adjustment methodology was unable to adjust O3 distributions such that they would meet the lower 

alternative standard level of 60 ppb. 

“0” counts denote non-zero estimates that round to zero. 

Total Ozone‐

Attributable Deaths

75ppb 75‐70 75‐65 75‐60

220 10 18 28

(‐310 ‐ 740) (‐13 ‐ 32) (‐24 ‐ 60) (‐39 ‐ 95)

230 7 14 23

(‐130 ‐ 570) (‐4 ‐ 17) (‐8 ‐ 35) (‐13 ‐ 59)

200 4 11 18

(‐290 ‐ 670) (‐6 ‐ 14) (‐16 ‐ 39) (‐25 ‐ 62)

270 8 20 40

(‐25 ‐ 550) (‐1 ‐ 18) (‐2 ‐ 41) (‐4 ‐ 83)

58 1 3 5

(‐190 ‐ 300) (‐4 ‐ 7) (‐10 ‐ 15) (‐17 ‐ 27)

520 18 33 54

(26 ‐ 990) (1 ‐ 35) (2 ‐ 64) (3 ‐ 110)

580 4 9 20

(110 ‐ 1000) (1 ‐ 8) (2 ‐ 17) (4 ‐ 37)

750 26 52 96

(‐310 ‐ 1800) (‐11 ‐ 62) (‐22 ‐ 130) (‐40 ‐ 230)

3200 150 740 NA

(1900 ‐ 4500) (92 ‐ 220) (440 ‐ 1000) NA

920 26 56 86

(200 ‐ 1600) (6 ‐ 46) (12 ‐ 100) (19 ‐ 150)

160 3 6 10

(‐170 ‐ 480) (‐3 ‐ 9) (‐6 ‐ 17) (‐11 ‐ 31)

350 15 31 49

(‐86 ‐ 770) (‐4 ‐ 33) (‐8 ‐ 70) (‐12 ‐ 110)

200 7 13 19

(‐280 ‐ 670) (‐10 ‐ 24) (‐18 ‐ 45) (‐26 ‐ 64)

210 4 9 14

(‐110 ‐ 520) (‐2 ‐ 10) (‐5 ‐ 23) (‐8 ‐ 37)

180 ‐13 8

(‐260 ‐ 610) (1 ‐ ‐2) (‐4 ‐ 10) (‐11 ‐ 27)

250 7 18 31

(‐23 ‐ 510) (‐1 ‐ 15) (‐2 ‐ 37) (‐3 ‐ 64)

56 0 1 5

(‐180 ‐ 290) (‐1 ‐ 1) (‐4 ‐ 7) (‐15 ‐ 25)

460 ‐17 ‐5 12

(23 ‐ 880) (‐1 ‐ ‐33) (0 ‐ ‐10) (1 ‐ 23)

600 ‐1 3 12

(110 ‐ 1100) (0 ‐ ‐1) (1 ‐ 6) (2 ‐ 22)

770 25 53 98

(‐320 ‐ 1800) (‐10 ‐ 60) (‐22 ‐ 130) (‐41 ‐ 240)

3000 96 500 NA

(1800 ‐ 4200) (57 ‐ 130) (300 ‐ 700) NA

820 14 33 51

(180 ‐ 1400) (3 ‐ 25) (7 ‐ 58) (11 ‐ 90)

160 3 5 9

(‐170 ‐ 490) (‐3 ‐ 8) (‐6 ‐ 17) (‐10 ‐ 28)

310 7 17 30

(‐77 ‐ 690) (‐2 ‐ 15) (‐4 ‐ 37) (‐7 ‐ 67)

2009 Simulation Year

Houston, TX

Los Angeles, CA

New York, NY

Philadelphia, PA

Sacramento, CA

St. Louis, MO

Atlanta, GA

Baltimore, MD

Boston, MA

Cleveland, OH

Denver, CO

Detroit, MI

New York, NY

Philadelphia, PA

Sacramento, CA

St. Louis, MO

Boston, MA

Cleveland, OH

Denver, CO

Detroit, MI

Houston, TX

Los Angeles, CA

Study Area

Air Quality Scenario

Atlanta, GA

Baltimore, MD

Change in Ozone‐Attributable Deaths

2007 Simulation Year
7-54 

Table 7-8. Percent of Total All-Cause Mortality Attributable to O3 and Percent Change in 

O3-Attributable Risk, 2007 and 2009 Air Quality. Smith et al. (2009) C-R functions, O3

season, CBSA-based study area, no threshold. 

NA: for NY, the model-based adjustment methodology was unable to adjust O3 distributions such that they would meet the lower 

alternative standard level of 60 ppb.

 

% of Baseline

Incidence

75ppb 75‐70 75‐65 75‐60

Atlanta, GA 1.1 4 8 13

Baltimore, MD 1.9 3 6 10

Boston, MA 1.2 2 5 9

Cleveland, OH 2.4 3 7 14

Denver, CO 0.8 2 5 9

Detroit, MI 3.0 3 6 10

Houston, TX 1.9 1 2 3

Los Angeles, CA 1.0 3 7 13

New York, NY 4.1 5 22 NA

Philadelphia, PA 3.2 3 6 9

Sacramento, CA 1.2 2 3 6

St. Louis, MO 2.5 4 9 14

Atlanta, GA 1.0 3 7 9

Baltimore, MD 1.8 2 4 7

Boston, MA 1.1 ‐0.3 2 4

Cleveland, OH 2.3 3 7 12

Denver, CO 0.8 0.3 2 8

Detroit, MI 2.7 ‐4 ‐1 3

Houston, TX 1.9 ‐0.1 0.5 2

Los Angeles, CA 1.1 3 7 13

New York, NY 4.0 3 16 NA

Philadelphia, PA 3.0 2 4 6

Sacramento, CA 1.2 2 3 6

St. Louis, MO 2.3 2 5 9

Study Area

Air Quality Scenario

% Change in O3‐Attributable

Risk

2007 Simulation Year

2009 Simulation Year
7-55 

Figure 7-2. Heat Maps for Short-term O3-attributable Mortality, 2007 Air Quality 

Adjusted to Just Meet the Existing Standard and Risk Reductions from Just Meeting 

Alternative Standards. Smith et al. (2009) C-R functions. (See Key at bottom of figure). 

NA: for NY, the model-based adjustment methodology was unable to adjust O3 distributions such that they would meet the lower 

alternative standard level of 60 ppb.

Key: For current standard (75) which is an absolute risk metric expressed as total O3-attributable deaths, color gradient ranges 

from blue (smallest O3-related mortality count) to red (highest O3-related mortality count). For estimates of decreases in risk, 

color gradient ranges from red (increase in risk – negative cell values) to blue (reduction in risk – positive cell values).

Current Standard (75)

Study area Daily 8hr Max Ozone Level (ppb) Total

0‐5 5‐10 10‐15 15‐20 20‐25 25‐30 30‐35 35‐40 40‐45 45‐50 50‐55 55‐60 60‐65 65‐70 70‐75 >75

Atlanta, GA 0 0 0 0 2 4 15 20 34 43 52 31 12 5 3 0 222

Baltimore, MD 0 0 0 0 1 6 11 22 43 37 36 38 23 6 5 2 228

Boston, MA 0 0 0 0 2 11 26 29 33 33 20 12 17 5 7 6 202

Cleveland, OH 0 0 0 1 3 9 25 41 55 50 27 25 19 8 6 0 268

Denver, CO 0 0 0 0 0 0 1 3 4 9 12 15 10 3 1 0 58

Detroit, MI 0 0 0 0 1 5 33 56 97 116 59 41 44 16 34 14 516

Houston, TX 0 0 0 0 14 42 107 124 126 81 42 42 2 0 0 0 580

Los Angeles, CA 0 0 0 0 0 0 0 10 204 268 233 27 8 3 0 0 753

New York, NY 0 0 0 0 24 113 341 625 851 545 418 268 45 0 0 0 3,230

Philadelphia, PA 0 0 0 2 0 25 46 115 157 175 155 122 75 31 7 7 916

Sacramento, CA 0 0 0 0 1 8 23 43 29 29 17 9 2 1 0 0 161

St. Louis, MO 0 0 0 1 2 6 15 52 53 61 60 38 24 23 10 3 348

Decrease 75 to 70

Study area Daily 8hr Max Ozone Level (ppb) Total

0‐5 5‐10 10‐15 15‐20 20‐25 25‐30 30‐35 35‐40 40‐45 45‐50 50‐55 55‐60 60‐65 65‐70 70‐75 >75 Inc. Dec.

Atlanta, GA 0 0 0 0 0 0 0 0 1 2 3 2 1 0 0 0 10 0 10

Baltimore, MD 0000000011121000706

Boston, MA 0000000001101000403

Cleveland, OH 0 0 0 0 0 0 0 0 1 2 1 2 1 1 0 0 8 0 10

Denver, CO 0000000000010000101

Detroit, MI 0 0 0 0 0 0 0 0 2 4 3 2 3 1 3 1 18 0 19

Houston, TX 0000 ‐1 ‐1 ‐10 2 2 2 2 0 0 0 0 4 ‐3 8

Los Angeles, CA 0 0 0 0 0 0 0 0 4 10 10 1 0 0 0 0 26 0 25

New York, NY 0000 ‐1 ‐2 0 14 31 37 41 29 6 0 0 0 154 ‐13 167

Philadelphia, PA 00000 ‐1 0 0 2 5 6 6 4 2 0 1 26 ‐2 27

Sacramento, CA 0000000011100000304

St. Louis, MO 0 0 0 0 0 0 0 1 2 3 3 2 2 2 1 0 15 0 16

Decrease 75 to 65

Study area Daily 8hr Max Ozone Level (ppb) Total

0‐5 5‐10 10‐15 15‐20 20‐25 25‐30 30‐35 35‐40 40‐45 45‐50 50‐55 55‐60 60‐65 65‐70 70‐75 >75 Inc. Dec.

Atlanta, GA 0 0 0 0 0 0 1 1 2 4 5 3 1 1 0 0 18 0 18

Baltimore, MD 0 0 0 0 0 0 0 0 2 2 3 4 2 1 1 0 14 0 15

Boston, MA 0 0 0 0 0 0 0 1 1 2 2 1 2 1 1 1 11 0 12

Cleveland, OH 0 0 0 0 0 0 0 1 4 4 3 3 3 1 1 0 20 ‐1 20

Denver, CO 0000000000111000303

Detroit, MI 000000 ‐1 0 3 7 5 4 5 2 5 2 33 ‐2 35

Houston, TX 0000 ‐2 ‐2 ‐30 4 4 3 4 0 0 0 0 9 ‐8 16

Los Angeles, CA 0 0 0 0 0 0 0 0 8 20 21 2 1 0 0 0 52 0 52

New York, NY 0000 ‐1 2 27 98 172 156 156 103 22 0 0 0 735 ‐7 742

Philadelphia, PA 00000 ‐1 ‐1 0 5 11 13 14 9 4 1 1 56 ‐4 60

Sacramento, CA 000000 ‐11 1 2 1 1 0 0 0 0 6 ‐1 6

St. Louis, MO 0 0 0 0 0 0 0 2 4 6 6 5 3 3 2 0 31 0 31

Decrease 75 to 60

Study area Daily 8hr Max Ozone Level (ppb) Total

0‐5 5‐10 10‐15 15‐20 20‐25 25‐30 30‐35 35‐40 40‐45 45‐50 50‐55 55‐60 60‐65 65‐70 70‐75 >75 Inc. Dec.

Atlanta, GA 0 0 0 0 0 0 1 2 4 6 7 5 2 1 1 0 28 0 29

Baltimore, MD 0 0 0 0 0 0 0 0 3 4 5 6 4 1 1 0 23 0 25

Boston, MA 0 0 0 0 0 0 0 1 2 3 3 2 3 1 2 1 18 0 19

Cleveland, OH 0 0 0 0 0 0 0 3 7 9 6 6 5 2 2 0 40 ‐2 41

Denver, CO 0000000000122100506

Detroit, MI 000000 ‐1 1 6 11 8 7 8 4 7 3 54 ‐2 57

Houston, TX 0000 ‐2 ‐4 ‐4 1 7 8 6 7 1 0 0 0 20 ‐11 31

Los Angeles, CA 0 0 0 0 0 0 0 1 24 35 29 4 1 1 0 0 96 0 95

New York, NY

Philadelphia, PA 00000 ‐1 ‐1 1 8 17 19 20 13 6 1 2 86 ‐4 89

Sacramento, CA 00000 ‐1 ‐1 2 3 3 2 1 0 0 0 0 10 ‐2 11

St. Louis, MO 0 0 0 0 0 0 0 4 6 9 10 7 5 5 2 1 49 0 49

Change in risk

Change in risk

Change in risk

NA
7-56 

Figure 7-3. Heat Maps for Short-term O3-attributable Mortality, 2009 Air Quality 

Adjusted to Just Meet the Existing Standard and Risk Reductions from Just Meeting 

Alternative Standards. Smith et al. (2009) C-R functions. (See Key at bottom of figure). 

NA: for NY, the model-based adjustment methodology was unable to adjust O3 distributions such that they would meet the lower 

alternative standard level of 60 ppb. 

Key: For current standard (75) which is an absolute risk metric expressed as total O3-attributable deaths, color gradient ranges 

from blue (smallest O3-related mortality count) to red (highest O3-related mortality count). For estimates of decreases in risk, 

color gradient ranges from red (increase in risk – negative cell values) to blue (reduction in risk – positive cell values).

Current Standard (75)

Study area Daily 8hr Max Ozone Level (ppb) Total

0‐5 5‐10 10‐15 15‐20 20‐25 25‐30 30‐35 35‐40 40‐45 45‐50 50‐55 55‐60 60‐65 65‐70 70‐75 >75

Atlanta, GA 0 0 1 2 7 13 15 28 41 37 24 25 8 1 0 0 201

Baltimore, MD 0 0 0 0 2 7 21 36 33 47 33 23 6 0 0 0 207

Boston, MA 0 0 0 0 7 14 26 33 29 31 27 4 2 3 5 2 183

Cleveland, OH 0 0 0 0 3 16 28 42 46 50 35 17 7 4 0 0 249

Denver, CO 0 0 0 0 0 1 2 3 6 12 15 13 4 1 0 0 56

Detroit, MI 0 0 1 7 5 21 36 53 89 116 30 40 36 0 17 5 456

Houston, TX 0 0 0 5 24 43 105 107 96 77 72 31 23 6 3 3 595

Los Angeles, CA 0 0 0 0 0 0 1 10 168 196 297 91 5 0 0 0 770

New York, NY 0 0 0 7 41 246 489 407 724 538 314 201 64 0 0 0 3,031

Philadelphia, PA 0 0 0 2 12 38 118 93 162 130 151 67 50 0 0 0 822

Sacramento, CA 0 0 0 0 1 10 28 30 32 24 18 14 3 0 0 0 162

St. Louis, MO 0 0 1 5 5 14 22 44 42 63 53 43 11 7 0 0 310

Decrease 75 to 70

Study area Daily 8hr Max Ozone Level (ppb) Total

0‐5 5‐10 10‐15 15‐20 20‐25 25‐30 30‐35 35‐40 40‐45 45‐50 50‐55 55‐60 60‐65 65‐70 70‐75 >75 Inc. Dec.

Atlanta, GA 0000000112221000709

Baltimore, MD 0000000011110000404

Boston, MA 0000 ‐1 0 ‐10 0 0 0 0 0 0 0 0 ‐1 ‐3 2

Cleveland, OH 0000000112210000707

Denver, CO 0000000000000000000

Detroit, MI 0 0 ‐1 ‐2 ‐1 ‐4 ‐4 ‐4 ‐4 ‐10 1 2 0 1 0 ‐17 ‐22 5

Houston, TX 000 ‐1 ‐2 ‐2 ‐3 ‐11 1 2 1 1 0 0 0 ‐1 ‐9 6

Los Angeles, CA 0 0 0 0 0 0 0 0 3 6 12 4 0 0 0 0 25 0 25

New York, NY 000 ‐1 ‐4 ‐16 ‐9 9 26 36 26 21 7 0 0 0 96 ‐44 139

Philadelphia, PA 0000 ‐1 ‐2 ‐2 ‐1 3 4 6 3 3 0 0 0 14 ‐6 21

Sacramento, CA 0000000011110000304

St. Louis, MO 000 ‐1 0 ‐10 0 1 2 2 2 1 0 0 0 7 ‐2 9

Decrease 75 to 65

Study area Daily 8hr Max Ozone Level (ppb) Total

0‐5 5‐10 10‐15 15‐20 20‐25 25‐30 30‐35 35‐40 40‐45 45‐50 50‐55 55‐60 60‐65 65‐70 70‐75 >75 Inc. Dec.

Atlanta, GA 0000 ‐1 ‐1 0 1 3 4 3 3 1 0 0 0 13 ‐2 15

Baltimore, MD 00000000132210009 ‐1 11

Boston, MA 0000 ‐1 ‐1 ‐10 1 1 2 0 0 0 1 0 3 ‐4 6

Cleveland, OH 00000 ‐1 0 2 3 5 4 3 1 1 0 0 18 ‐1 21

Denver, CO 0000000000010000101

Detroit, MI 0 0 ‐1 ‐3 ‐1 ‐5 ‐4 ‐3 ‐23 1 4 4 0 2 1 ‐5 ‐21 16

Houston, TX 000 ‐1 ‐4 ‐4 ‐5 ‐12 3 5 3 3 1 1 0 3 ‐15 19

Los Angeles, CA 0 0 0 0 0 0 0 0 6 14 25 8 0 0 0 0 53 0 53

New York, NY 000 ‐1 ‐5 ‐19 18 60 122 138 93 72 24 0 0 0 500 ‐48 550

Philadelphia, PA 0000 ‐2 ‐3 ‐3 ‐1 8 8 13 7 6 0 0 0 33 ‐11 44

Sacramento, CA 00000 ‐10 1 2 2 1 1 0 0 0 0 5 ‐2 7

St. Louis, MO 000 ‐1 ‐1 ‐1 0 1 2 5 5 5 1 1 0 0 17 ‐4 22

Decrease 75 to 60

Study area Daily 8hr Max Ozone Level (ppb) Total

0‐5 5‐10 10‐15 15‐20 20‐25 25‐30 30‐35 35‐40 40‐45 45‐50 50‐55 55‐60 60‐65 65‐70 70‐75 >75 Inc. Dec.

Atlanta, GA 0000 ‐1 ‐1 0 2 4 5 4 4 2 0 0 0 19 ‐2 21

Baltimore, MD 00000 ‐1 0 1 2 5 4 3 1 0 0 0 14 ‐2 16

Boston, MA 0000 ‐1 ‐1 ‐11 1 3 3 1 0 0 1 0 8 ‐4 11

Cleveland, OH 0 0 0 0 0 0 1 4 5 8 7 4 2 1 0 0 31 ‐1 33

Denver, CO 0000000000121000505

Detroit, MI 0 0 ‐1 ‐4 ‐2 ‐6 ‐4 ‐2 1 8 3 6 6 0 4 1 12 ‐22 32

Houston, TX 000 ‐2 ‐6 ‐6 ‐6 0 4 7 9 5 5 1 1 1 12 ‐22 35

Los Angeles, CA 0 0 0 0 0 0 0 1 19 26 37 13 1 0 0 0 98 0 97

New York, NY

Philadelphia, PA 000 ‐1 ‐2 ‐4 ‐3 0 12 12 19 10 8 0 0 0 51 ‐14 65

Sacramento, CA 00000 ‐1 ‐11 3 3 2 2 0 0 0 0 9 ‐2 11

St. Louis, MO 0 0 ‐1 ‐2 ‐1 ‐1 0 3 4 8 8 7 2 1 0 0 30 ‐6 34

Change in risk

Change in risk

Change in risk

NA
7-57 

Figure 7-4. Short-Term O3-attributable All-Cause Mortality for 2007 (top panel) and 2009 

(bottom panel) Air Quality Adjusted to Just Meet the Existing and Alternative Standards. 

Smith et al. (2009) C-R functions. 

 

2007 Simulation year

2009 Simulation year

0

2

4

6

8

10

12

14

16

18

20

75ppb 70ppb 65ppb 60ppb

Total ozone‐related mortality per 100,000 residents

Trend in ozone‐related mortality across standard

levels (deaths per 100,000)

Atlanta, GA

Baltimore, MD

Boston, MA

Cleveland, OH

Denver, CO

Detroit, MI

Houston, TX

Los Angeles, CA

New York, NY

Philadelphia, PA

Sacramento, CA

St. Louis, MO

0

2

4

6

8

10

12

14

16

18

20

75ppb 70ppb 65ppb 60ppb

Total ozone‐related mortality per 100,000 residents

Trend in ozone‐related mortality across standard levels

(deaths per 100,000)

Atlanta, GA

Baltimore, MD

Boston, MA

Cleveland, OH

Denver, CO

Detroit, MI

Houston, TX

Los Angeles, CA

New York, NY

Philadelphia, PA

Sacramento, CA

St. Louis, MO
7-58 

Table 7-9. Short-Term O3-attributable Morbidity Counts, Percent of Baseline and 

Reduction in O3-attributable Risk, Respiratory-Related Hospital Admissions, 2007 and 

2009 Air Quality. 

NA: for NY, the model-based adjustment methodology was unable to adjust O3 distributions such that they would meet the lower 

alternative standard level of 60 ppb. 

“0” counts denote non-zero estimates that round to zero. 

Total Ozone‐

Attributable

Counts

Percent of

Baseline

75ppb 75‐70 75‐65 75‐60 75ppb 75‐70 75‐65 75‐60

HA (respiratory); Detroit (Katsouyanni et al.,  2009)

1hr max, penalized splines 190 10 18 29 2.8 5 10 15

1hr max, natural splines 180 9.8 18 28 2.7 5 10 15

HA (respiratory); NYC  (Silverman and Ito, 2010; Lin et al., 2008)

HA  Chronic Lung Disease (Lin) 140 7.9 34 3.3 5 23

HA  Asthma (Silverman) 490 33 140 27.7 5 21

HA  Asthma, PM2.5 (Silverman) 360 23 98 20.2 5 22

1hr max penalized splines 480 11 23 36 2.4 2 5 7

HA (COPD less asthma); all 12 study areas (Medina‐Ramon, et al., 2006)

Atlanta, GA 55 3 5 8 2.5 5 9 15

Baltimore, MD 40 1 3 5 2.6 4 7 12

Boston, MA 58 1 3 6 2.2 2 6 9

Cleveland, OH 37 1 3 6 2.4 4 8 17

Denver, CO 18 1 1 2 2.9 3 6 11

Detroit, MI 71 2 4 7 2.5 3 6 10

Houston, TX 57 1 2 3 2.1 1 3 6

Los Angeles, CA 110 5 10 15 2.7 4 9 13

New York, NY 200 13 57 NA 2.2 6 28 NA

Philadelphia, PA 97 3 7 11 2.5 3 7 11

Sacramento, CA 15 1 1 2 2.5 3 7 11

St. Louis, MO 43 2 4 7 2.6 5 10 15

HA (respiratory); Detroit (Katsouyanni et al.,  2009)

1hr max, penalized splines 170 2.8 10 20 2.5 2 6 11

1hr max, natural splines 160 2.7 9.8 19 2.4 2 6 11

HA (respiratory); NYC  (Silverman and Ito, 2010; Lin et al., 2008)

HA  Chronic Lung Disease (Lin) 140 5.9 25 3.2 4 17

HA  Asthma (Silverman) 470 28 110 27.3 4 17

HA  Asthma, PM2.5 (Silverman) 350 20 79 19.9 4 18

HA (respiratory); LA (Linn et al., 2000)

1hr max penalized splines 500 11 23 37 2.4 2 4 7

HA (COPD less asthma); all 12 study areas (Medina‐Ramon, et al., 2006)

Atlanta, GA 52 3 4 6 2.2 5 8 12

Baltimore, MD 37 1 2 3 2.3 2 5 8

Boston, MA 53 0 1 2 2.0 0 1 4

Cleveland, OH 36 1 3 5 2.2 3 8 14

Denver, CO 18 0 1 2 2.7 1 4 11

Detroit, MI 64 ‐3 ‐1 1 2.2 ‐4 ‐2 1

Houston, TX 63 0 1 3 2.2 1 2 5

Los Angeles, CA 120 5 10 16 2.7 4 8 13

New York, NY 190 8 40 NA 2.1 4 20 NA

Philadelphia, PA 88 2 4 6 2.3 2 4 7

Sacramento, CA 16 1 1 2 2.4 3 7 11

St. Louis, MO 41 2 3 5 2.4 3 8 12

2009 Simulation Year

2007 Simulation Year

HA (respiratory); LA (Linn et al., 2000)

NA NA

NA NA

Air Quality Scenario

% Change in Ozone‐Related

Risk

Endpoint/Study Area/Descriptor

Change in Ozone‐Attributable

Counts
7-59 

Table 7-10. Short-Term O3-attributable Morbidity Counts, Percent of Baseline and 

Reduction in O3-attributable Risk, Emergency Department Visits, 2007 and 2009 Air 

Quality.

NA: for NY, the model-based adjustment methodology was unable to adjust O3 distributions such that they would meet the lower 

alternative standard level of 60 ppb. 

 

Total Ozone‐

Attributable

Counts

Percent of

Baseline

75ppb 75‐70 75‐65 75‐60 75ppb 75‐70 75‐65 75‐60

ER Visits (repiratory); Atlanta (Strickland et al., 2007)

Distributed lag 0‐7 days 6,600 350 650 1,000 19.6 4 8 13

Average day lag 0‐2 3,900 200 370 580 11.6 5 8 13

ER‐visits (respiratory); Atlanta  (Tolbert et al., 2007, Darrow et al., 2011)

Tolbert 7,000 310 580 920 5.8 4 8 12

Tolbert‐CO 6,300 280 510 810 5.1 4 8 12

Tolbert‐NO2 5,700 250 460 730 4.6 4 8 12

Tolbert‐PM10 4,400 200 360 570 3.6 4 8 12

Tolbert‐PM10, NO2 4,300 190 350 550 3.5 4 8 12

Darrow 3,800 170 310 490 3.1 4 8 12

ER‐visits (asthma); NYC   (Ito et al, 2007)

single pollutant model 11,000 620 2,700 19.9 5 22

PM2.5 8,300 480 2,100 15.5 5 22

NO2 6,800 390 1,700 12.8 5 23

CO 11,000 660 2,900 21.0 5 22

SO2 8,500 490 2,200 16.1 5 22

ER Visits (repiratory); Atlanta (Strickland et al., 2007)

Distributed lag 0‐7 days 5,900 270 490 700 17.2 4 7 10

Average day lag 0‐2 3,500 150 280 400 10.1 4 7 10

ER‐visits (respiratory); Atlanta  (Tolbert et al., 2007, Darrow et al., 2011)

Tolbert (single pollutant 6,400 230 440 620 5.1 3 6 9

Tolbert‐CO 5,700 200 390 550 4.5 3 6 9

Tolbert‐NO2 5,200 180 350 500 4.1 3 6 9

Tolbert‐PM10 4,100 140 270 390 3.2 3 6 9

Tolbert‐PM10, NO2 3,900 140 260 380 3.1 3 6 9

Darrow  (single pollutant 3,500 120 230 330 2.8 3 6 9

ER‐visits (asthma); NYC   (Ito et al, 2007)

single pollutant model 10,000 470 2,100 19.3 4 17

PM2.5 8,100 360 1,600 15.1 4 17

NO2 6,700 290 1,300 12.4 4 18

CO 11,000 500 2,200 20.4 4 17

SO2 8,300 370 1,700 15.5 4 17

2009 Simulation Year

NA NA

NA NA

Endpoint/Study Area/Descriptor

Air Quality Scenario

% Change in Ozone‐Related

Risk

2007 Simulation Year

Change in Ozone‐Attributable

Counts
7-60 

Table 7-11. Short-Term O3-attributable Morbidity Counts, Percent of Baseline and 

Reduction in O3-attributable Risk, Asthma Exacerbations, 2007 and 2009 Air Quality.

a

 previous day; b same day

 

Total Ozone‐

Attributable

Counts

Percent of

Baseline

75ppb 75‐70 75‐65 75‐60 75ppb 75‐70 75‐65 75‐60

Asthma exacerbation (wheeze); Boston (Gent et al., 2003, 2004)

  Chest Tightness (1hr max) 40,000 1,200 3,300 5,100 28.9 2 5 9

  Chest Tightness (8hr max) 30,000 680 1,900 3,000 21.2 2 5 8

  Chest Tightness (1hr max, PM2.5)a 41,000 1,200 3,300 5,100 29.1 2 5 9

  Chest Tightness (1hr max, PM2.5)b 38,000 1,100 3,000 4,700 26.9 2 5 9

  Shortness of Breath (1hr max) 29,000 800 2,200 3,400 16.3 2 6 10

  Shortness of Breath (8hr max) 35,000 780 2,100 3,400 19.6 2 5 8

  Wheeze (PM2.5) 76,000 2,200 6,000 9,300 23.3 2 6 9

Asthma exacerbation (wheeze); Boston (Gent et al., 2003, 2004)

  Chest Tightness (1hr max) 38,000 290 1,400 2,800 27.0 0.4 2 5

  Chest Tightness (8hr max) 28,000 ‐110 470 1,300 19.8 ‐0.4 1 3

  Chest Tightness (1hr max, PM2.5)a 38,000 300 1,400 2,900 27.2 0.4 2 5

  Chest Tightness (1hr max, PM2.5)b 35,000 270 1,300 2,600 25.1 0.4 3 5

  Shortness of Breath (1hr max) 27,000 190 930 1,900 15.1 1 3 6

  Shortness of Breath (8hr max) 32,000 ‐120 540 1,500 18.3 ‐0.4 1 4

  Wheeze (PM2.5) 71,000 530 2,600 5,200 21.7 0.5 3 6

2009 Simulation Year

Endpoint/Study Area/Descriptor

Air Quality Scenario

% Change in Ozone‐Related

Risk

2007 Simulation Year

Change in Ozone‐Attributable

Counts
7-61 

Figure 7-5. Short-Term O3-attributable Respiratory Hospital Admissions, 2007 (top panel) 

and 2009 (bottom panel) Air Quality Adjusted to Meet the Existing and Alternative 

Standards. Medina-Ramon, et al. (2006) C-R functions.

 

2007 Simulation year

2009 Simulation year

4

6

8

10

12

14

16

75ppb 70ppb 65ppb 60ppb

Total ozone‐related HA per 100,000

Trend in ozone‐related HA across standard levels

(HA per 100,000)

Atlanta, GA

Baltimore, MD

Boston, MA

Cleveland, OH

Denver, CO

Detroit, MI

Houston, TX

Los Angeles, CA

New York, NY

Philadelphia, PA

Sacramento, CA

St. Louis, MO

4

6

8

10

12

14

16

75ppb 70ppb 65ppb 60ppb

Total ozone‐related HA per 100,000

Trend in ozone‐related HA across standard levels

(HA per 100,000)

Atlanta, GA

Baltimore, MD

Boston, MA

Cleveland, OH

Denver, CO

Detroit, MI

Houston, TX

Los Angeles, CA

New York, NY

Philadelphia, PA

Sacramento, CA

St. Louis, MO
7-62 

Table 7-12. Long-Term O3-attributable Respiratory Mortality, 2007 and 2009 Air Quality. 

Jerrett et al. (2009) C-R functions, CBSA-based study area, no threshold. 

NA: for NY, the model-based adjustment methodology was unable to adjust O3 distributions such that they would meet the lower 

alternative standard level of 60 ppb. 

 

Absolute Ozone

Atrributable

Mortality

75ppb 75‐70 75‐65 75‐60

590 35 64 100

(210 ‐ 920) (12 ‐ 59) (22 ‐ 110) (34 ‐ 160)

390 17 35 57

(140 ‐ 610) (6 ‐ 29) (12 ‐ 57) (19 ‐ 93)

640 20 53 82

(230 ‐ 1000) (7 ‐ 33) (18 ‐ 88) (28 ‐ 140)

330 16 35 64

(120 ‐ 510) (6 ‐ 27) (12 ‐ 58) (22 ‐ 100)

330 13 26 43

(120 ‐ 500) (4 ‐ 21) (9 ‐ 44) (15 ‐ 71)

600 28 50 78

(220 ‐ 940) (10 ‐ 46) (17 ‐ 82) (27 ‐ 130)

460 8.0 16 27

(160 ‐ 720) (3 ‐ 13) (5 ‐ 26) (9 ‐ 44)

1,500 82 160 240

(560 ‐ 2400) (28 ‐ 140) (54 ‐ 260) (83 ‐ 400)

2,100 140 550

(750 ‐ 3300) (47 ‐ 230) (190 ‐ 900)

930 42 87 130

(330 ‐ 1400) (14 ‐ 69) (30 ‐ 140) (44 ‐ 210)

300 14 26 44

(110 ‐ 470) (5 ‐ 22) (9 ‐ 43) (15 ‐ 73)

480 27 56 84

(170 ‐ 750) (9 ‐ 45) (19 ‐ 92) (29 ‐ 140)

550 32 59 82

(200 ‐ 860) (11 ‐ 53) (20 ‐ 98) (28 ‐ 140)

360 12 27 41

(130 ‐ 560) (4 ‐ 20) (9 ‐ 44) (14 ‐ 68)

580 3.7 23 47

(210 ‐ 920) (1 ‐ 6) (8 ‐ 38) (16 ‐ 77)

300 14 32 50

(110 ‐ 470) (5 ‐ 24) (11 ‐ 53) (17 ‐ 82)

320 5.8 18 45

(120 ‐ 490) (2 ‐ 10) (6 ‐ 30) (16 ‐ 75)

540 ‐6.7 14 38

(190 ‐ 850) (‐2 ‐ ‐11) (5 ‐ 23) (13 ‐ 64)

490 11 24 40

(180 ‐ 770) (4 ‐ 18) (8 ‐ 40) (14 ‐ 66)

1,600 77 160 250

(570 ‐ 2400) (26 ‐ 130) (54 ‐ 260) (84 ‐ 400)

2,000 120 420

(730 ‐ 3200) (40 ‐ 200) (140 ‐ 690)

850 31 66 97

(310 ‐ 1300) (11 ‐ 52) (23 ‐ 110) (33 ‐ 160)

310 14 28 44

(110 ‐ 480) (5 ‐ 24) (9 ‐ 46) (15 ‐ 73)

440 19 41 66

(160 ‐ 690) (6 ‐ 31) (14 ‐ 67) (23 ‐ 110)

NA

NA

2009 Simulation Year

Houston, TX

Los Angeles, CA

New York, NY

New York, NY

Philadelphia, PA

Sacramento, CA

St. Louis, MO

Philadelphia, PA

Sacramento, CA

St. Louis, MO

Atlanta, GA

Baltimore, MD

Boston, MA

Cleveland, OH

Denver, CO

Detroit, MI

Study Area

Air Qualtiy Scenario

Atlanta, GA

Baltimore, MD

Change in Ozone‐Attributable Mortality

2007 Simulation Year

Los Angeles, CA

Boston, MA

Cleveland, OH

Denver, CO

Detroit, MI

Houston, TX
7-63 

Table 7-13. Long-Term O3-attributable Respiratory Mortality Percent of Baseline 

Incidence and Percent Reduction in O3-attributable Risk, 2007 and 2009 Air Quality. 

Jerrett et al. (2009) C-R functions, CBSA-based study area, no threshold. 

NA: for NY, the model-based adjustment methodology was unable to adjust O3 distributions such that they would meet the lower 

alternative standard level of 60 ppb. 

 

% of Baseline

Incidence

75ppb 75‐70 75‐65 75‐60

Atlanta, GA 18.6 5 9 14

Baltimore, MD 18.8 4 7 12

Boston, MA 17.2 3 7 11

Cleveland, OH 17.7 4 9 16

Denver, CO 20.8 3 6 11

Detroit, MI 18.4 4 7 11

Houston, TX 16.3 1 3 5

Los Angeles, CA 20.4 4 8 13

New York, NY 16.9 6 23 NA

Philadelphia, PA 18.4 4 8 12

Sacramento, CA 17.8 4 7 12

St. Louis, MO 18.8 5 10 15

Atlanta, GA 17.0 5 9 13

Baltimore, MD 17.4 3 6 10

Boston, MA 16.0 1 3 7

Cleveland, OH 16.8 4 9 14

Denver, CO 20.0 1 5 12

Detroit, MI 17.0 ‐12 6

Houston, TX 16.9 2 4 7

Los Angeles, CA 20.7 4 8 13

New York, NY 16.7 5 18 NA

Philadelphia, PA 17.2 3 6 10

Sacramento, CA 18.0 4 7 12

St. Louis, MO 17.7 3 8 12

Study Area

Air Quality Scenario

% Change in O3‐Attributable

Risk

2007 Simulation Year

2009 Simulation Year
7-64 

Figure 7-6. Long-Term O3-attributable Respiratory Mortality for 2007 and 2009 Air 

Quality Adjusted to Just Meet the Existing and Alternative Standards, Jerrett et al. (2009) 

C-R functions. 

 

2007 Simulation Year

2009 Simulation Year

0

5

10

15

20

25

30

35

75ppb 70ppb 65ppb 60ppb

Total ozone‐related mortality per 100,000 residents

Trend in ozone‐related mortality across standard

levels (deaths per 100,000)

Atlanta, GA

Baltimore, MD

Boston, MA

Cleveland, OH

Denver, CO

Detroit, MI

Houston, TX

Los Angeles, CA

New York, NY

Philadelphia, PA

Sacramento, CA

St. Louis, MO

0

5

10

15

20

25

30

75ppb 70ppb 65ppb 60ppb

Total ozone‐related mortality per 100,000 residents

Trend in ozone‐related mortality across standard

levels (deaths per 100,000)

Atlanta, GA

Baltimore, MD

Boston, MA

Cleveland, OH

Denver, CO

Detroit, MI

Houston, TX

Los Angeles, CA

New York, NY

Philadelphia, PA

Sacramento, CA

St. Louis, MO
7-65 

The presentation of key observations drawn from review of the core risk estimates is 

divided into two sections: (1) the assessment of health risks associated with just meeting the 

existing standard (section 7.5.1) and (2) the assessment of risk changes from meeting alternative 

standards relative to meeting the existing standard (section 7.5.2). The presentation of key 

observations in each of these two sections is further separated into those associated with (a) 

short-term O3-attributable mortality, (b) short-term O3-attributable morbidity and (c) long-term 

O3-attributable mortality. Unless otherwise noted, all risk estimates discussed in these three 

sections are core risk estimates. In some cases we refer to the confidence intervals around risk 

estimates. When an effect estimate is drawn from a study with low statistical power, confidence 

intervals can be wide, and can include negative values because of the assumptions of normality 

in the distribution of the effect estimate. Negative lower-confidence bounds do not imply that 

additional exposure to O3 has a beneficial effect, but rather that the estimated O3 effect estimate 

in the C-R function was not statistically significantly different from zero, and thus has a higher 

degree of uncertainty as to the magnitude of the estimated risk. As noted earlier, presentation of 

sensitivity analysis results and their use in interpreting the core risk estimates is covered in 

section 7.5.3. 

7.5.1 Assessment of Health Risk after Adjusting Air Quality to Just Meet the Existing 

Standard 

The analysis of risk after simulating just meeting the existing standard focuses on 

absolute risk, since this is of greatest relevance in evaluating the adequacy of the existing 

standard. 

Short-term O3-attributable mortality 

 After adjusting air quality to just meet the existing standard, estimates of O3-related 

all-cause mortality range across urban study areas from 58 to 3,200 deaths (for 

simulation year 2007) and from 56 to 3,000 deaths (for simulation year 2009) (see 

Table 7-7). This translates into from 0.8 to 4.1% of baseline all-cause mortality (for 

simulation year 2007) and from 0.8 to 4.0% (for simulation year 2009) (see Table 

7-8) in these study areas. Generally, O3-attributable all-cause mortality risks continue 

to be lower for the 2009 simulation year as compared with the 2007 simulation year 

(with the exception of Houston), reflecting the generally lower ambient O3 levels 

associated with 2009 for most of the study areas (see Table 7-7 and Table 7-8).

 Confidence intervals (CIs) reflecting the statistical fit of the effect estimates used in 

modeling risk demonstrate substantial variability across the 12 urban study areas. In 
7-66 

general, the upper 95th percentile CI tends to be from 2-3 times larger than the point 

estimate for the 12 urban study areas (see Table 7-7). However, some study areas 

have wider confidence intervals (e.g., for Denver the upper CI is about 5 times the 

point estimate), while others have tighter relative CIs (e.g., New York, where the 

upper CI is ~1.4 times larger than the point estimate). This variation in the CIs 

associated with risk estimates can reflect a number of factors including the statistical 

power of the underlying epidemiological study, which is based on the population size, 

and differences in the magnitude of such factors as exposure measurement error and 

correlations between O3 and other pollutants. 

After just meeting the existing O3 standard for simulation year 2007, all-cause 

mortality estimates based on C-R functions from Smith et al. (2009) continue to be 

driven largely by days with total O3 levels within 30 to 70 ppb, with 87 to 99% of the 

mortality estimate across the 12 urban study areas associated with days in this range. 

A smaller fraction (9 to 24%) of the mortality risk is associated with days above 60 

ppb, for most of the study areas (see Figure 7-2, “Existing standard (75)” plot).35 For 

2009, this pattern continues although risk distributions are shifted downward, 

reflecting the lower ambient O3 levels generally seen in this simulation year 

compared with 2007(see Figure 7-3, “current standard (75)” plot). For 2009, 9% to 

33% of O3-attributable mortality risk is associated with days having O3 measurements 

55-60 ppb or higher. Approximately 0% to 2% of total mortality estimates for the 

existing standard air quality scenario are associated with days having ambient O3

levels of 20 ppb or less.36

 Estimates of O3-attributable respiratory-related HA range from tens to hundreds of 

cases (after adjusting air quality to just meet the existing standard) depending on the 

type of respiratory HA endpoint modeled and the specific urban study areas evaluated 

 

35 Houston, LA, NY, and Sacramento study areas have a significantly smaller percentage (<1%) of its estimated 

mortality associated with days above 60ppb. 36 In the first draft O3 HREA, we included consideration for surrogate LMLs (based on the lowest composite monitor 

values used in modeling short-term exposure-related mortality for each urban study area – see Table 7-5, First 

Draft HREA, U.S. EPA, 2012). For the 8-hr max monitoring season LML (applicable to the Smith et al., 2009-

based core risk estimate generated for this HREA), we have values ranging from 4 to 17 ppb and from 5 to 16 ppb 

(across the 12 urban study areas for 2007 and 2009, respectively). If we look at heat maps characterizing the 

distribution of short-term exposure-related mortality for recent conditions (see “recent conditions” heat maps in 

Figures 7B-1 and 7B-2 in Appendix 7B) we see that the majority of O3-related mortality falls above these 

surrogate LML ranges. Consequently we see that had we integrated consideration for the surrogate LMLs into 

modeling of short-term exposure-related mortality, there would have been small changes in estimated risk. 
7-67 

(see Table 7-9). All 12 urban study areas were modeled for one of more respiratoryrelated HA endpoints. 

 O3-attributable ER (for respiratory symptoms) ranged into the thousands for both 

New York and Atlanta when considering simulated air quality that just meets the 

existing standard (these were the only two study areas modeled for this health 

endpoint) (see Table 7-10). 

 Estimates of O3-attributable asthma exacerbation (wheeze) in Boston are in the tens 

of thousands to over 100,000 (see Table 7-11). The percent of baseline for this health 

endpoint after adjusting air quality to just meet the existing standard ranges from 

about 20 to 30%, a risk estimate higher than that estimated for the other short-term 

morbidity endpoints evaluated here (see Table 7-11 and compare to values in 7-9 and 

7-10). 

Long-term O3-attributable mortality 

 After simulating air quality that just meet the existing standard, estimates of O3-

related respiratory mortality ranges across the urban study areas from 300 to 2,100 

deaths (for 2007) and from 300 to 2,000 deaths (for 2009) (see Table 7-12). This 

translates into from 16.3 to 20.8% of baseline across the 12 urban study areas (for 

2007) and from 16 to 20.7% (for 2009) using the Jerrett et al. (2009) C-R nationalscale function applied to each urban area (see Table 7-13). As discussed in section 

7.3.2, because of the long-term exposure metric (seasonal mean of daily maximum 8-

hr O3 concentrations) employed in risk modeling, there is the potential for overlap 

between short-term and long-term exposure-related mortality estimates. For that 

reason, these two categories of mortality estimates cannot be considered distinct and 

should not be added to estimate total mortality. 

95th percentile CIs for long-term O3-attributable respiratory mortality suggest greater 

power (and potential less heterogeneity) associated with modeling this health endpoint, 

compared with short-term O3-attributable mortality. None of the CIs for long-term O3-

attributable mortality include negative estimates as lower bounds (see Table 7-12). 7.5.2 

7.5.2 Assessment of Health Risk after Adjusting Air Quality to Just Meet Alternative 

Standards 

As discussed earlier, we have considered three alternative standard levels (70, 65 and 60 

ppb), each evaluated using the same form and averaging time of the existing standard. In 
7-68 

presenting risk estimates associated with air quality adjusted to just meet each of these 

alternative standard levels, we focus on the change in risk associated with a comparison of O3

levels after simulation of the existing standard with levels after simulation of each of the 

alternative standard levels. This is of greatest relevance in comparing the potential public health 

benefit associated with each of the alternative standards relative to the level of protection 

afforded by just meeting the existing standard. 

In reviewing these risk estimates, it is important to keep in mind that simulation of 

alternative standard levels is based on a reaching the 4th highest daily maximum 8-hr average, or 

peak-based metric. Based on the simulated air quality information for the 12 urban study areas, 

there is a tendency for modeled O3 to increase on lower concentration days and decrease on 

higher concentration days.37 Therefore, it is not immediately clear that we would expect risk 

reductions with increasing stringency in peak-based standard levels when applying C-R 

functions that are based on the full distribution of daily maximum 8-hr values. Specifically, risk 

reductions are only expected to the extent that the composite monitor daily maximum 8-hr 

concentrations decrease as lower alternative standards are simulated. As discussed in Chapter 4, 

after adjustment to alternative standard levels, decreases in O3 typically occur on higher O3 days 

which tend to occur during warmer (summer) months and are concentrated in suburban areas. 

Conversely, increases in O3, typically occur lower O3 days which tend to occur in the cooler 

portions of the year and are focused in core urban areas. In general, variability in predicted daily 

O3 concentrations decreases when meeting lower standard levels. 

Short-term O3-attributable mortality 

 In our analysis, the mortality risk metric is moderately responsive to adjusted air 

quality that just meets the existing and alternative standard levels. This is related to 

(1) how O3 concentrations respond to reductions in NOx emissions used to meet the 

standards, and (2) how the risk metrics are associated with temporal and spatial 

patterns of O3. As discussed in section 7.1.1, mortality risk is modeled using 

composite monitor values (i.e., averages of O3 measurements across monitors in an 

urban study area) which removes spatial variability in measured O3 within an urban 

study area (also removing variability in changes in O3 across an urban area resulting 

from NOx reductions). Furthermore, in modeling total mortality risk for the core 

analysis, we add the risk changes occurring across all days within the monitored O3

 

37 This relationship is also observed in ambient air quality measurements as discussed in Chapter 4 and appendices. 
7-69 

season, including days with low values of O3 as well as days with high values of O3. 

This means that we include both decreases in risk on those days when O3 is estimated 

to decrease (generally occurring on days with higher values of O3) and increases in 

risk when O3 is simulated to increase (generally associated with lower values of O3). 

The dampened response of short-term mortality risk can be contrasted with clinical 

study-based risk estimates. The clinical study-based estimates primarily reflect 

changes in the upper end of the O3 distribution where we tend to see more consistent, 

progressive reductions in exposures of concern and health risk coincide with 

progressive increases in the stringency of alternative standard levels. In addition, 

clinical-based estimates of risk are based on detailed micro-environmental exposure 

modeling which uses individual monitor values instead of composite monitor values, 

thereby resulting is less dampening of spatial variability in O3 within a given urban 

study area. 

 Generally, the magnitude of risk reduction increases as lower alternative standard 

levels are simulated. For example, for the lowest alternative standard we evaluated, 

60 ppb, across the 12 urban study areas, we predict from 5 to 96 fewer O3-attributable 

deaths for simulation year 2007 (relative to estimated risk associated with air quality 

that just meets the existing standard) (see Table 7-7). This range is from 5 to 98 

deaths for simulation year 2009. These ranges (for the 60 ppb standard level) translate 

into a 2 to 14% reduction in O3-attributable risk relative to estimated risk associated 

with air quality that just meets the existing standard (see Table 7-8). 

 As noted in section 7.1.1, some of the urban study areas are projected to experience 

increases in O3 (and hence risk) when adjusting air quality that just meets the existing 

standard and some of the alternative standard levels. Focusing specifically on the 

alternative standard levels, we see that, for the core analysis, this potential increase in 

risk only occurs for the 2009 simulation year and specifically for three of the urban 

study areas (Boston, Detroit and Houston – see Table 7-7). For example, Detroit is 

estimated to have an increase of 17 O3-attributable deaths after meeting the 70 ppb 

standard (when compared to risk remaining after meeting the existing standard). 

However, we estimate a net reduction of 12 O3-attributable deaths in this study area 

after meeting the 60 ppb level (again based on comparison to risk after meeting the 

existing standard). Furthermore, for all three urban study areas with initial risk 

increases (based on comparing meeting the existing standard to meeting alternative 

standards), we see that these increases are offset after meeting the lowest alternative 
7-70 

standard simulated (60 ppb) (see Table 7-7). The potential for risk increases is 

increased somewhat for several of the urban study areas when we simulate how the 

O3 distribution shifts from recent conditions to just meeting the existing standard (see 

Appendix 7B, Tables 7B-1 and 7B-2). Specifically, in simulating estimated risk from 

moving from recent conditions to just meeting the existing standard, we see that for 

the 2007 simulation year, two of the study areas (Houston and Los Angeles) have risk 

increases after meeting the existing standard compared to recent ambient conditions 

while half of the twelve urban study areas have risk increases for the 2009 simulation 

year in adjusting air quality to meet the existing standard relative to recent conditions. 

It is also important to keep in mind that, for the urban study areas of New York and 

Los Angeles, there are additional uncertainties in the simulation of existing and 

alternative standards given the limitations in the application of the adjustment 

methodology to very large emissions reductions and that the 95th percent confidence 

interval lower bound estimate of hourly O3 concentrations was used to capture a 

scenario in which these urban study areas could meet lower standard levels (65 ppb 

for New York and 60 ppb for Los Angeles). In five of these eight cases, the initial 

risk increases (including the increase in going from recent ambient conditions to air 

quality just meeting the existing standard) is fully offset after meeting the lowest 

alternative standard level (60 ppb).38

 Figure 7-4 provides plots of short-term mortality risk associated with air quality that 

just meets the existing and alternative standards adjusting for total exposed 

population (i.e., O3-attributable deaths per 100,000 exposed). Total O3-attributable 

risk, even when adjusted for population, varies substantially across the 12 urban study 

areas, with New York and Philadelphia having the highest estimated risk and Atlanta 

and Denver the lowest. This spread in risk (adjusted for population) reflects, to a great 

extent, differences in the effect estimates used in modeling this endpoint for each 

study area, which can in turn reflect a number of factors (e.g., differences in behavior 

such as outdoor activity across cities and differences in exposure measurement error). 

However, despite considerable variability in absolute O3-attributable risk, Figure 7-4 

also suggests that most of the study areas display moderate reductions in O3-

 

38 For both LA and Houston (in 2007) and Houston (2009) a modest net risk increase still persists (compared to risk 

under recent conditions), even when we have simulated the lowest alternative standard considered (60 ppb) (see 

Tables 7B-1 and 7B-2). 
7-71 

attributable risk across the three alternative standards (with the exception of New 

York, which has a notable decrease in risk for the 70 to 65 ppb standard level).39 This 

suggests that a substantial fraction of O3-attributable risk would still remain, even 

after simulating air quality that just meets the lowest alternative standard considered. 

 Heat map plots of risk reductions for 2007 suggest that most of the risk reductions 

associated with simulation of all three alternative standards occur on days with 

composite O3 level between 35 and 60 ppb (see Figure 7-4). By contrast, most of the 

risk increases occur on days with composite O3 levels between 20 and 35ppb (see 

Figure 7-4). This is expected given that most of the increases in urban core O3 are 

associated with lower O3 days where NOx titration is prevalent (see Appendix 4D, 

section 4.6, Figures 40-54). Very little of the projected change in risk (increases, or 

decreases) for any of the alternative standards considered occurred on days with O3

levels below 20 ppb O3. Similar observations hold for risk results generated for 

simulation year 2009. 

Short-term O3-attributable morbidity 

 Generally, because the short-term O3 exposure-related morbidity endpoints use the 

same air metrics as used in modeling short-term O3-attributable mortality (i.e., 8-hr 

maximum and 8-hr mean) the pattern of risk reduction seen for these morbidity 

endpoints are similar to those seen with short-term mortality (see Table 7-9 through 

Table 7-11 and Figure 7-5). However, New York, as mentioned with regard to shortterm O3-attributable mortality, has substantially higher percent reductions (for O3-

attributable risk) compared with the other study areas. For example, with ER visits 

(asthma), under the 65 ppb alternative standard in simulation year 2007, New York is 

estimated to have a 22 to 23% reduction in the number of ER-visits associated with 

O3 exposure (see Table 7-10). 

Long-term O3-attributable mortality 

Although long-term O3-attributable mortality is modeled using a different O3 metric 

(essentially a long-term trend in the 1-hr maximum for the hottest two seasons – see section 

7.3.2) the overall magnitude and pattern of reduction in O3-related risk is similar to that seen 

 

39 With the New York urban study area, we recognize however that there is significant uncertainty associated with 

the use of the CBSA-based study area due to significant heterogeneity in short-term O3-attributable mortality 

effect estimates (from Smith et al., 2009) within that larger urban study area (see discussion in section 7.6.1). 
7-72 

with short-term exposure related mortality. Specifically, for the 2007 simulation year, for most 

urban study areas risk reductions range from 11 to 16% (for the 60 ppb standard) (see Table 

7-13). Risk reductions are generally slightly smaller across alternative standard levels for 

simulation year 2009. For the 2009 simulation year, for Detroit, we see a relatively small risk 

increase for the 70 ppb alternative standard (compared to risk under the existing standard). 

However that initial increase is offset by risk reductions for the other (lower) alternative standard 

levels simulated (see Table 7-13). 

7.5.3 Sensitivity Analyses Designed to Enhance Understanding of the Core Risk Estimates 

We have completed a number of sensitivity analyses intended to support interpretation of 

the core risk estimates. These sensitivity analyses, which are described in section 7.4.3, can be 

divided into two categories: (a) sensitivity analyses exploring factors impacting air quality 

characterization (specifically composite monitor composition) and (b) sensitivity analyses 

exploring the impact of alternative C-R function specifications. As noted in section 7.4.3, we 

also completed an initial influence analysis designed to identify which of the input factors to the 

risk model (for short-term exposure-related mortality) are primarily responsible for inter-city 

variability in that risk metric. This section summarizes the results of these sensitivity analyses 

and presents key observations related to those analyses, beginning with the influence analysis 

and then proceeding to sensitivity analyses focused on air quality characterization and alternative 

C-R function specification. 

Influence analysis 

The influence analysis considered three factors involved in modeling risk for the shortterm exposure-related mortality endpoint including: baseline incidence, composite monitor O3

levels and Bayes-adjusted city-specific effect estimates (recall that the core risk estimate is based 

on effect estimates derived as part of analyses published in Smith et al., 2009). Each of these 

input factors displays inter-study area variation and are responsible, collectively, for 

heterogeneity in risk estimates.40 In completing the analysis, we first calculated a central 

tendency estimate of risk based on the mean of each input factor across the 12 urban study areas 

for the 2009 simulation year (i.e., using the average of the city-specific values for each of the 

input factors). We then systematically varied each of the three heterogeneity-related factors 

(effect estimate, composite monitor-based O3 level and baseline incidence) to one standard 

 

40 Note, that the demographic count input factor also varies across the study areas and is an important factor in 

determining total O3-attributable mortality. However, for the influence analysis, we used deaths per 100,000 as the 

risk metric which standardizes on demographic count and therefore allowed us to exclude this input parameter in 

conducting the influence analysis. 
7-73 

deviation (SD) above its mean value (reflecting variance across the 12 urban study area values) 

and noted the percent increase produced by that perturbation over the initial mean risk estimate. 

This influence analysis allowed us to explore the impact of both model form – specifically, 

potential non-linearities in the model – as well as the relative magnitude of variability in each of 

the three heterogeneity-related input factors on risk. The influence analysis generated the 

following results: baseline incidence (23%), composite monitor-based O3 level (10%), and effect 

estimate (54%). In other words, the 54% result for effect estimate means that use of a value 1 SD 

over the mean (for the effect estimate) in generating risk, resulted in a risk estimate that was 54% 

larger than the risk estimate based on the mean of all input factors. These results clearly show 

that, of the three input factors considered, the effect estimate is primarily responsible for intercity variability in short-term exposure-related risk. 

Interestingly, when we look at the coefficient of variation (CV) for these three 

heterogeneity-related input factors we see values almost identical to the influence analysis results 

in terms of relative magnitude to each other (i.e., 0.230, 0.085, and 0.507 for baseline incidence, 

composite monitor-based O3 levels and effect estimate, respectively). Given that the CV values 

only reflect variability in each input factor and not model form (i.e., do not reflect potential nonlinearities in the model), the fact that the CV values almost exactly match the influence analysis 

results in terms of relative magnitude suggest that there is very little if any non-linearity in the 

model calculations involving these three input factors. Had non-linearity existed to a significant 

extent, then the influence analysis results would have differed substantially from the CV results. 

The fact that both analyses suggest a primary role for the effect estimate in driving inter-city 

variability in risk emphasizes the importance of the sensitivity analyses exploring alternative C-R 

functions specifications that were completed for the HREA (see below). 

Air quality-related sensitivity analyses 

This category of sensitivity analysis covers (a) the use of a smaller study area (the Smith 

et al., 2009 study areas) as contrasted with the CBSA-based study areas used in the core analysis, 

and (b) the use of alternative approaches to simulate air quality that just meets the existing and 

alternative standards (for a subset of the study areas) (see section 7.4.3 for additional detail). This 

category of sensitivity analysis was applied to short-term O3-attributable mortality given the 

importance of the endpoint in the policy-context.41

 

41 Observations regarding the sensitivity of core short-term O3-attributable mortality risk to these sensitivity analyses 

can be applied with care to the core short-term O3-attributable morbidity endpoints, since many of these used 

similar air quality metrics in modeling risk. 
7-74 

To allow for easier visual comparisons, we have presented the results of this sensitivity 

analysis category in graphical form (see Figure 7-7, numerical results are presented in Appendix 

7C). This figure presents point estimates and 95th percentile confidence ranges for the core model 

and for two sensitivity analyses: (a) SA1 (use of the smaller Smith et al., 2009 based study area) 

and (b) SA2 (use of the alternative approach to adjusting air quality). SA2 is not presented for all 

of the study areas, only for the subset included in these alternative simulations (see section 

7.4.3). The sensitivity analyses results presented in Figure 7-7 are the changes in O3-related risk 

that result from meeting the three alternative standards relative to meeting the existing standard. 

Furthermore, these changes reflect deaths per 100,000, which standardizes the estimates on 

population. This removes variation in the size of the underlying exposed population as a factor to 

consider in interpreting these results. 

For the sensitivity analysis examining use of the smaller Smith et al. (2009) study area, 

we have also included heat maps similar to those used in conveying core estimates for short-term 

exposure related mortality (see section 7.5 for a description of the heat maps used in the core 

analysis). These heat maps (included in Appendix 7C – see Figure 7C-1) allow us to consider 

how changes in risk, including both reductions in risk and increases in risk are distributed across 

the O3 air quality distributions for each study area. 

Key observations related to the air quality-related sensitivity analyses include: 

 Use of smaller study area reduces magnitude of risk reduction: For most of the 

study areas, use of the smaller Smith et al. (2009)-based study area resulted in smaller 

risk reductions (again expressed in terms of changes in deaths per 100,000). For 

example, in Figure 7-7 (Baltimore plot), we see that estimated change in risk for SA1 

(the smaller study area) are lower than estimated change in risk for the core scenario. 

This likely reflects the mix of monitors in the smaller study areas which results in a 

smaller change in the composite monitor value (for the existing standard versus 

alternative standard levels) as compared with composite monitor values based on the 

larger CBSA study area. However, it is important to keep the relatively small 

magnitude of these risk reductions in mind when considering the results of the 

sensitivity analysis. Most of these differences in risk reductions are less than 1 

individual per 100,000 which reflects the fact that total risk reduction (for short-term 

O3-attributable mortality) across the urban study areas is relatively small (see Table 

7-7). 

 Reductions in risk are focused on higher O3 days while increases are focused on 

lower O3 days: Figure 7C-1 allows us to consider patterns in risk reductions and 

increases when using the smaller Smith et al., 2009-based study areas in modeling 
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risk. Figure 7C-1 (particularly the plots of risk decreases) suggests that decreases in 

risk tend to occur on days with composite monitor O3 concentrations ranging from 

40-70ppb, while increases in risk tend to occur on days with composite monitor 

values in the range at or below 30-40 ppb (with most risk increases falling in the 

range of 15ppb to 40ppb). As noted in 7.1.1, there is less confidence in specifying the 

nature of the C-R function (and therefore less confidence in specifying risk) in the 

range below 20 ppb. 

 Application of effect estimates derived for smaller study areas to larger CBSAbased study areas: As noted in section 7.3.2, in those instances where an 

epidemiological study provides effect estimates for multiple subareas within a larger 

CBSA-based study area, we are selecting the effect estimates that represent the 

largest number of individuals to model that CBSA-based study areas. There is 

uncertainty associated with this approach. Specifically, as illustrated in Table 7-3, 

effect estimates within some of the CBSA-based study areas can display considerable 

heterogeneity. For example, consider the Smith et al. (2009)-based effect estimates 

that fall within the CBSA-based New York study areas (these vary from 0.0001 to 

0.0009 – almost a 10 fold factor, see Table 7-3). Furthermore, with the CBSA-based 

New York study area, Smith et al. (2009)-based effect estimates only cover about half 

of the total population, with 8.3 million residents living within portions of the CBSA 

not covered by Smith et al. (2009)-based effect estimates. As noted in section 7.3.2, 

in these types of situations, we have decided to use the single effect estimates 

representing the largest number of residents in modeling the larger CBSA-study area. 

This reflects the observation that, in the case of the New York CBSA, one of the 

available effect estimates (for the New York study area), represents ~7 times the 

population of the other effect estimates (see Table 7-3). In the case of the Los 

Angeles CBSA, there is significantly less difference between the available effect 

estimates, making the issue of heterogeneity (and the specification of a single effect 

estimate for this study area) less important. Never the less, we recognize that the issue 

of heterogeneity does complicate extrapolation of effect estimates for smaller study 

areas to the larger CBSA study areas modeled in this analysis and does introduce a 

degree of uncertainty that is difficult to characterize. 

 Use of alternative approach for simulating air quality that just meets existing 

and alternative standard levels: Use of an alternative approach to simulate air 

quality that just meets the existing and alternative standard levels did not produce a 

consistent trend in terms of changes in risk between existing and alternative standards 

relative to the core analysis. For example, if we look at Figure 7-7 (plot for Houston), 
7-76 

we see that SA2 (reflecting application of the alternative simulation approach) has a 

larger risk reduction than the core estimate. By contrast, if we look at the plot for Los 

Angeles, we see that the SA2 risk change is lower than the core estimate. Again, as 

with the sensitivity analysis results looking at study area size, it is important to keep 

in mind that the magnitude of these differences is relatively small, reflecting the small 

magnitude of mortality risk associated with these analyses in general (see Table 7-7). 

It is also important to note that in the alternative simulation approach, the HDDMadjustment approach assumed the same percent reductions of NOx and VOC and did 

not examine if a different air quality distribution could have been obtained with a 

different combination of NOx versus VOC reductions. For most of the urban areas, 

the percent NOx and VOC reductions were very similar to the NOx-only percent 

reductions. The similarity in the NOx reductions between the two approaches could be 

the reason for there being little difference in the risk estimates between the core and 

the alternative approach. 

Sensitivity analyses related to specification of C-R functions 

This category of sensitivity analysis covers a number of factors related to the 

specification of C-R functions for both short-term O3-attributable and long-term O3-attributable 

mortality. In the case of short-term O3-attributable mortality, we consider (a) the use of Bayes 

adjusted effect estimates using regional priors (as contrasted with the Bayes adjusted values 

using a national prior applied in the core analysis), (b) the use of a co-pollutants model 

considering PM10 (as contrasted with the single pollutant model used in the core analysis) and (c) 

application of effect estimates from Zanobetti and Schwartz (2008) reflecting a summer focused 

analysis (as contrasted with the Smith et al., 2009-based analysis reflecting the entire monitoring 

period in each study area, which is used in the core analysis). 

For long-term O3-attributable mortality, we consider the use of regionally-differentiated 

single pollutant effect estimates obtained from Jerrett et al. (2009), as contrasted with the single 

national co-pollutants model used in the core analysis (see section 7.1.1). In addition, we present 

estimates for long-term O3 attributable mortality based on application of results from a national 

level single pollutant model. We have also included a simulation of the impact of potential 

thresholds in the relationship between long-term O3 exposure and respiratory-related mortality. 

Specifically, we have modeled risk using alternative effect estimates reflecting the application of 

a range of potential thresholds (40, 45, 50, 55, 56 and 60 ppb) included in Jerrett et al. (2009) 

(see Sasser, 2014) and compared those estimates with estimates based on non-thresholds models 

included as core estimates (see section 7.3.2). 
7-77 

For sensitivity analyses examining alternative specification of the C-R function for shortterm O3-attributable mortality, we have used the same graphical approach as used in presenting 

results of the sensitivity analyses examining air quality characterization (i.e., plots of point 

estimates with 95th percentile C.I.s for the core and sensitivity analyses for each of the study 

areas – see Figure 7-8). Here we also plot estimates of risk changes using deaths per 100,000 to 

standardize in terms of total exposed population. 

For the sensitivity analysis considering alternative C-R functions for long-term O3-

attributable mortality, we present results in both tabular and graphical formats. Results of 

sensitivity analyses exploring the impact of regional-differentiated effect estimates and a national 

O3-only effect estimate are presented in Table 7-14 and Table 7-15, respectively. Each table 

includes both (a) the percent of baseline mortality attributable to O3 (considering air quality 

adjusted to just meet the existing standard) and (b) the percent reduction in O3-attributable risk 

for each of the alternative standard levels for both the core and sensitivity analysis scenarios. 

Results of the sensitivity analysis exploring the impact of potential thresholds in long-term O3-

attributable mortality are presented in tabular form in Figure 7-9. In that figure, we include 

separate plots for each of the air quality scenarios with each plot including estimates of O3-

attributable mortality (as deaths per 100,000) for non-threshold and a range of threshold models. 

Key observations related to sensitivity analyses examining alternative C-R functions 

specifications for both short-term and long-term exposure-related mortality include: 

 Use of regional Bayes-adjusted effect estimates in modeling short-term O3-

attributable mortality: The use of Bayes-adjusted effect estimates with regional 

priors in modeling short-term O3-attributable mortality, had a mixed impact across the 

urban study areas, with some study areas having increased changes in risk and others 

having smaller changes, relative to the core analysis. For example, in Figure 7-8 (plot 

for Baltimore), SA1 had a larger change in risk compared with the core analysis. 

However, as with the sensitivity analyses examining air quality-related factors 

(discussed above), it is important to keep in mind that the overall magnitude of the 

O3-attributable mortality risk is relatively small and that these differences in changes 

in risk (comparing SA1 to the core analysis) are generally in the fraction of a person 

per 100,000 exposed population. 

 Use of a co-pollutants model (with PM10) in modeling short-term O3-attributable 

mortality: The use of the PM10 co-pollutant model in modeling short-term O3-

attributable mortality (as contrasted with the single pollutant model used in the core 

analysis) tended to have a relatively small effect on estimates of risk changes for the 

alternative standards considered. For example, in Figure 7-8 (plot for Boston), we see 

that the estimates of risk changes for SA2 (reflecting application of the PM10 co-
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pollutant model) is essentially the same as the core risk estimate. It is important to 

keep in mind that the PM10 co-pollutant model suffers from significantly reduced 

power due to the 1/3 to 1/6 day sampling frequency used in measuring PM10 (this 

reduces the number of observations available to support epidemiological analysis). 

This has the impact of greatly increasing the confidence intervals on the SA2 risk 

estimates relative to the core estimates. 

 Use of Zanobetti and Schwartz (2008) effect estimates in modeling short-term 

O3-attributable mortality: The use of Zanobetti and Schwartz (2008) effect 

estimates (reflecting a focus on the warmer summer months) produces a mixed set of 

results when compared to the core risk estimates. If we look at Figure 7-8 we see that, 

for Boston, estimates of risk changes for SA3 (reflecting application of the Zanobetti 

and Schwartz, 2008 effect estimates) are significantly larger than core estimates. By 

contrast, SA3 estimates of risk changes for Houston are significantly smaller than the 

core estimates. It is important, however to keep in mind that the Zanobetti and 

Schwartz (2008) effect estimates will tend to under-estimate total risk since they only 

model impacts during the summer months (while the Smith et al., 2009 effect 

estimates allow us to model impacts for the entire O3 monitoring season in each study 

area). Note that if the O3 effect were only occurring during the summer months, then 

the total risk estimated using effect estimates from the two studies would be similar. 

However, because the risks in many locations are smaller (using the Zanobetti and 

Schwartz, 2008 based effect estimates), this suggests that a significant portion of the 

O3 effect occurs outside of the summer months evaluated in this study. 

 Use of regional-differentiated effect estimates in modeling long-term O3-

attributable mortality: Risk estimates generated using regional-specific effect 

estimates for long-term O3-attributable mortality differ substantially from the core 

estimates based on a single national-level effect estimate (see Table 7-14). 

Furthermore, the risk estimates generated using the regional effect estimates display 

considerable variability (see Table 7-14) reflecting the significant variability in the 

underlying effect estimates (see Jerrett et al., 2009, Table 4). The regional effect 

estimates range from 0.99 (for the Northeast) to 1.21 (for the Southwest) and include 

1.00 (no O3 effect for the Industrial Midwest). As noted earlier in section 7.5, 

negative risk estimates should not be interpreted as suggesting that O3 exposure is 

beneficial. Rather, these suggest that there may be instability in the underlying 

estimates or that potential confounding has not been fully addressed. Regional effect 

estimates used in this analysis have considerably larger confidence intervals than the 

national estimate (compare values in Jerrett et al., 2009 Table 3 with values in Table 
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4). This suggests that the regional estimates are less stable than the national estimates 

and are subject to considerably greater uncertainty. For this reason, while the results 

of this sensitivity analysis point to the potential for regional heterogeneity in the longterm O3-attributable mortality effect estimate, we do not have significant confidence 

in the regionally-based risk estimates themselves given the relatively large confidence 

intervals associated with those estimates. 

 Use of national-based single pollutant model in modeling long-term O3-

attributable mortality: Risk estimates generated using the national-level O3-only 

effect estimate were significantly lower (~30%) than the core risk estimates which 

utilize a co-pollutants model (which includes PM2.5) (see Table 7-15). In this case, 

control for another pollutant results in a stronger O3 signal, possibly due to an 

association between PM2.5 and a confounder or effect modifier associated with the 

O3-related effect. 

 Consideration for potential thresholds in the relationship between long-term O3

exposure and respiratory-related mortality: The results of the sensitivity analysis 

based on the suite of threshold-based effect estimates suggests that compared to the 

estimates generating by using a linear (no-threshold) model, these models can result 

in substantially lower estimates of O3-attributable mortality across all of the standard 

levels considered (see Figure 7-9 and Appendix 7C, Tables 7C-8 through 7C-12). For 

example, in Figure 7-9 we see that, for where air quality was adjusted to just meet the 

existing standard (i.e., the ‘Current Standard 75’ plot), estimates of risk across the 

study areas using a model that includes a 40 ppb threshold (i.e., see ‘T40’ identifier 

along X-axis) are 60-90% less than risks estimated using a non-threshold models (i.e., 

see ‘NT86’ and ‘NT96’ identifiers along X-axis). For most of the study areas, 

estimated risk is progressively less when using models with increasing threshold 

levels (i.e., ‘T45’ through ‘T60’ models), with all study areas showing no O3-

attributable risk when using a model that includes a 60 ppb threshold (‘T60’ in Figure 

7-9). This overall pattern is also evident when estimating risks associated with air 

quality adjusted to each of the lower alternative standard levels (Figure 7-9).
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Figure 7-7. Sensitivity Analysis: Effect of Air Quality Factors on Short-Term O3-attributable Mortality, 2

SA1-smaller (Smith et al., 2009-based) study area, SA2-alternative method for simulating standards. 
7-81 

Figure 7-8. Sensitivity Analysis: Effect of C-R Function Specification on Short-Term O3-attributable Mor

Quality. SA1-regional Bayes adjustment, SA2-co-pollutant model (PM10), SA3-Zanobetti and Schwartz-ba
7-82 

Table 7-14. Sensitivity Analysis for Long-Term O3-attributable Respiratory Mortality, 

Alternative C-R Function Specification (regional effect estimates), 2009 Air Quality. 

Percent of baseline all-cause mortality and change in O3-attributable risk, Jerrett et al. 

(2009), O3 season. 

NA: for NY, the model-based adjustment methodology was unable to adjust O3 distributions such that they would meet the lower 

alternative standard level of 60 ppb.

 

% of Baseline

Incidence

75ppb 75‐70 75‐65 75‐60

Atlanta, GA 17.0 5 9 13

Baltimore, MD 17.4 3 6 10

Boston, MA 16.0 1 3 7

Cleveland, OH 16.8 4 9 14

Denver, CO 20.0 1 5 12

Detroit, MI 17.0 ‐12 6

Houston, TX 16.9 2 4 7

Los Angeles, CA 20.7 4 8 13

New York, NY 16.7 5 18 NA

Philadelphia, PA 17.2 3 6 10

Sacramento, CA 18.0 4 7 12

St. Louis, MO 17.7 3 8 12

Atlanta, GA 41.3 4 8 11

Baltimore, MD ‐6.9 4 9 13

Boston, MA ‐6.1 1 5 9

Cleveland, OH 0.0 0 0 0

Denver, CO 27.5 1 4 11

Detroit, MI 0.0 0 0 0

Houston, TX 41.2 2 3 6

Los Angeles, CA 4.6 3 7 11

New York, NY ‐6.5 7 23 NA

Philadelphia, PA ‐6.7 4 9 13

Sacramento, CA 24.9 4 7 11

St. Louis, MO 0.0 0 0 0

Study Area

Air Quality Scenario

% Change in O3‐Attributable

Risk

Core analysis(2009)

Sensitivity analysis(regional effect estimates) (2009)
7-83 

Table 7-15. Sensitivity Analysis for Long-Term O3-attributable Respiratory Mortality, 

Alternative C-R Function Specification (national O3-only effect estimates), 2009 Air 

Quality. Percent of baseline all-cause mortality and change in O3-attributable risk, Jerrett 

et al. (2009), O3 season. 

NA: for NY, the model-based adjustment methodology was unable to adjust O3 distributions such that they would meet the lower 

alternative standard level of 60 ppb. 

 

% of Baseline

Incidence

75ppb 75‐70 75‐65 75‐60

Atlanta, GA 17.0 5 9 13

Baltimore, MD 17.4 3 6 10

Boston, MA 16.0 1 3 7

Cleveland, OH 16.8 4 9 14

Denver, CO 20.0 1 5 12

Detroit, MI 17.0 ‐12 6

Houston, TX 16.9 2 4 7

Los Angeles, CA 20.7 4 8 13

New York, NY 16.7 5 18 NA

Philadelphia, PA 17.2 3 6 10

Sacramento, CA 18.0 4 7 12

St. Louis, MO 17.7 3 8 12

Atlanta, GA 11.9 5 9 13

Baltimore, MD 12.2 3 6 10

Boston, MA 11.2 1 3 7

Cleveland, OH 11.8 4 9 14

Denver, CO 14.1 1 5 12

Detroit, MI 11.9 ‐12 6

Houston, TX 11.9 2 4 7

Los Angeles, CA 14.6 4 8 13

New York, NY 11.7 5 18 NA

Philadelphia, PA 12.1 3 7 10

Sacramento, CA 12.6 4 8 12

St. Louis, MO 12.4 4 8 13

Sensitivity analysis(ozone‐only effect estimates) (2009)

Study Area

Air Quality Scenario

% Change in O3‐Attributable

Risk

Core analysis(2009)
7-84 

Figure 7-9. Sensitivity Analysis: Long-Term O3-attributable Respiratory Mortality 

(threshold models: O3-only effect estimates), 2009 Air Quality. Each figure presents results 

for a particular standard level illustrating the effect of alternative threshold models on O3-

attributable risk across the 12 urban study areas – values are O3-attributable 

deaths/100,000. NT86 and NT96 indicate non-thresholds models based on the 86 and 96 city 

datasets, respectively. T# models are models reflecting threshold by ppb level. (Jerrett et 

al., 2009 and Sasser, 2014). 

0

5

10

15

20

25

NT86 NT96 T40 T45 T50 T55 T56 T60

Deaths per 100,000

Model (NT: no threshold, T#: threshold in ppb)

LT Mortality 2009 (Baseline)

Atlanta, GA

Baltimore, MD

Boston, MA

Cleveland, OH

Denver, CO

Detroit, MI

Houston, TX

Los Angeles, CA

New York, NY

Philadelphia, PA

Sacramento, CA

St. Louis, MO

0

5

10

15

20

25

NT86 NT96 T40 T45 T50 T55 T56 T60

Deaths per 100,000

Model (NT: no threshold, T#: threshold in ppb)

LT Mortality 2009 (Current Standard 75)

Atlanta, GA

Baltimore, MD

Boston, MA

Cleveland, OH

Denver, CO

Detroit, MI

Houston, TX

Los Angeles, CA

New York, NY

Philadelphia, PA

Sacramento, CA

St. Louis, MO

0

5

10

15

20

25

NT86 NT96 T40 T45 T50 T55 T56 T60

Deaths per 100,000

Model (NT: no threshold, T#: threshold in ppb)

LT Mortality 2009 (Alternative Standard 70)

Atlanta, GA

Baltimore, MD

Boston, MA

Cleveland, OH

Denver, CO

Detroit, MI

Houston, TX

Los Angeles, CA

New York, NY

Philadelphia, PA

Sacramento, CA

St. Louis, MO

0

5

10

15

20

25

NT86 NT96 T40 T45 T50 T55 T56 T60

Deaths per 100,000

Model (NT: no threshold, T#: threshold in ppb)

LT Mortality 2009 (Alternative Standard 65)

Atlanta, GA

Baltimore, MD

Boston, MA

Cleveland, OH

Denver, CO

Detroit, MI

Houston, TX

Los Angeles, CA

New York, NY

Philadelphia, PA

Sacramento, CA

St. Louis, MO

0

5

10

15

20

25

NT86 NT96 T40 T45 T50 T55 T56 T60

Deaths per 100,000

Model (NT: no threshold, T#: threshold in ppb)

LT Mortality 2009 (Alternative Standard 60)

Atlanta, GA

Baltimore, MD

Boston, MA

Cleveland, OH

Denver, CO

Detroit, MI

Houston, TX

Los Angeles, CA

New York, NY

Philadelphia, PA

Sacramento, CA

St. Louis, MO
7-85 

7.6 KEY OBSERVATIONS 

This section discusses our overall confidence associated with risk estimates presented in 

this HREA. We begin by presenting a set of key observations related to overall confidence in the 

risk assessment. These observations are drawn largely from (a) consideration for the systematic 

approach used in designing the risk assessment, (b) our assessment of the degree to which we 

have captured key sources of variability in the analysis (section 7.4.1) (c) our qualitative 

assessment of uncertainty in the risk assessment (section 7.4.2), and (d) the results of the 

sensitivity analyses completed (section 7.5.3). Once we present these observations, we provide a 

synthesis statement reflecting our overall degree of confidence in the risk estimates (at the end of 

this section). Key observations addressing overall confidence in the analysis include: 

 A deliberative process was used in specifying each of the analytical elements 

comprising the risk model. This is in line with recommendations made by the 

National Research Council in Science and Decisions, Advancing Risk Assessment

(NRC, 2009. p. 89-90) for improving risk assessment as applied in the regulatory 

context. This deliberative process included first identifying specific goals for the 

analysis, and then designing the analysis to meet those goals, given available 

information and methods. Specific analytical elements reflected in the design include: 

selection of urban study areas, characterization of ambient air O3 levels, selection of 

health endpoints to model and selection of epidemiological studies (and specification 

of C-R functions) (see sections 7.1.1 and 7.3). In addition, the design of this HREA 

reflects consideration for comments provided by the public and by CASAC in their 

review of the draft HREAs (Frey, and Samet 2012; Frey, 2014). 

 Review of available literature in the O3 ISA(U.S. EPA. 2013a) for short-term 

exposure-related mortality, resulted in a decision not to incorporate a true (no effect) 

threshold into our risk modeling. However, the studies used to develop the C-R 

functions specifically for short-term exposure-related mortality indicate a range of 

ambient O3 (area-wide daily levels, based on averaging across monitors in locations 

with multiple monitors, of ≤ 20 ppb) below which there is reduced confidence in 

specifying the nature of the C-R relationship (see section 7.1.1). Only a relatively 

small fraction of short-term O3-attributable mortality reflected in the risk estimates is 

associated with days in this range with the vast majority of the risk estimates 

reflecting days with peak O3 measurements well above this level (see section 7.5.1 

and 7.5.2). 

 Modeling of short-term O3-attributable mortality utilized Bayes-adjusted city-specific 

effect estimates (see section 7.1.1 and section 7.3.2). These effect estimates are 
7-86 

considered to have increased overall confidence since they combine elements of the 

local city-specific signal with a broader scale (national) signal. 

 Sensitivity analyses exploring alternative C-R functions for modeling short-term O3-

attributable mortality (e.g., Bayes regional prior based estimates, co-pollutants 

models) suggested that alternative models can have a moderate impact on risk (see 

section 7.5.3). This impact reflects primarily the relatively small magnitude of shortterm O3-attributable mortality reductions associated with air quality adjusted to just 

meet the alternative standard levels. 

 The use of alternative C-R functions for modeling long-term O3-attributable mortality 

(specifically the regional-based estimates referenced earlier) was shown to have a 

significant impact on risk (see section 7.5.3). However, concerns over the power and 

hence stability of the regional effect estimates used in this simulation limit our ability 

to draw firm conclusions regarding the potential magnitude of that regional 

heterogeneity. Estimates of mortality risk attributable to long-term O3 exposure are 

highly sensitive to the existence of a threshold (see section 5.3). 

 Use of CBSA-based study areas in modeling all health endpoints in order to address 

known bias associated with using smaller study areas. As discussed in 7.1.1, we have 

used larger CBSA-based study areas to avoid focusing the risk assessment only on 

core urban areas (often used in the epidemiological studies providing effect estimates) 

which can experiences increases in O3 based on simulated air quality that just meets 

the existing and alternative standard levels. There is uncertainty in using effect 

estimates based on smaller study areas to represent larger CBSA-based study areas 

(see section 7.4.2 and 7.5.3). A key concern is heterogeneity in the effect estimates 

which may suggest increased uncertainty in applying effect estimates to larger study 

areas (since larger study areas may display heterogeneity in the nature of the 

relationship between O3 exposure and risk). It is possible also that this heterogeneity 

varies across urban areas, or regionally. For both categories of mortality endpoints 

(short-term and long-term O3-attributable), potential heterogeneity in the mortality 

effect even within larger urban areas remains a potentially important source of 

uncertainty. 

 Specifically in relation to short-term exposure-related mortality and morbidity which 

depend on time-series studies, there is uncertainty in applying effect estimates derived 

based on evaluating the longitudinal (in terms of time) relationship between ambient 

O3 and a particular health effect to the modeling of a discrete shift in the entire 

distribution that occurs when you simulate an alternative standard. Specifically, the 

time-series studies relate unit changes in day to day O3 with a degree of impact on 
7-87 

baseline health effect rates. In the risk assessment, we use this effect estimate to 

predict risk for a unit shift in daily composite monitor value. There is uncertainty in 

this application of the effect estimates, although it is not possible at this time to 

characterize either qualitatively, or quantitatively the magnitude of this uncertainty 

and the degree of any potential bias that could be introduced into the simulation of 

risk. 

 Use of HDDM-adjustment approach to simulate air quality that just meets the 

existing and alternative standard levels provides more refined estimates of ambient O3

distributions given its ability to characterize the physical and chemical processes of 

O3 formation in the atmosphere. However, in the case of both the New York and Los 

Angeles study areas, given the limitations in the application of the adjustment 

methodology to very large emissions perturbations and the need to use the 95th

percent confidence interval lower bound estimate to simulate air quality that just 

meets of these standard levels, we have reduced overall confidence in the simulation 

of the O3 concentrations for these study areas and consequently all health endpoints 

modeled for risk for these two study areas (see section 7.4.2 and 7.5.3). 

Based on the key observations regarding confidence presented above, we draw the 

following conclusions regarding overall confidence in the risk estimates generated for this 

HREA. We have a reasonable degree of confidence in short-term O3-attributable mortality and 

morbidity estimates for ten of the twelve study areas. This confidence is tempered somewhat by 

concerns over potential heterogeneity in effect estimates for mortality which can impact the risk 

assessment given our use of larger CBSA-based study areas. Our confidence in risk estimates 

generated for both New York and Los Angeles urban study areas is considerably lower than for 

the remaining ten study areas due to (a) concerns over air quality modeling (specifically the use 

of lower-bound fits to the DDM model) and (b) specifically in the case of New York, evidence 

for significant heterogeneity in the mortality effect estimates for subareas within the CBSA. We 

have somewhat lower confidence in our estimates of mortality risk attributable to long-term O3

exposures, primarily because there is only a single well designed study, and because of the large 

impact of uncertainty around the existence and potential location of a threshold in the C-R 

function for this endpoint. In addition, as with short-term O3-attributable mortality, overall 

confidence is further tempered by concerns over regional heterogeneity in the O3 effect. If we 

had regionally-differentiated effect estimates for this endpoint that had sufficient power and 

stability, we would consider using these as the basis for generating core risk estimates (rather 

than the national-level effect estimate used in the current analysis). 

 
7-88 

7.7 REFERENCES 

Abt Associates Inc. 1996. A Particulate Matter Risk Assessment for Philadelphia and Los 

Angeles. Prepared for Office of Air Quality Planning and Standards. Research Triangle 

Park, NC: EPA Office of Air and Radiation, OAQPS, July 1996. Available at: 

<http://www.epa.gov/ttnnaaqs/standards/pm/data/jly3amd.pdf>. 

Abt Associates, Inc. 2010. Environmental Benefits and Mapping Program (Version 4.0). 

Prepared for U.S. Environmental Protection Agency, Bethesda, MD. Research Triangle 

Park, NC: EPA Office of Air Quality Planning and Standards. Available on the Internet 

at: <http://www.epa.gov/air/benmap>. 

Akinbami, L.J.; C.D. Lynch; J.D. Parker and T.J. Woodruff. 2010. The association between 

childhood asthma prevalence and monitored air pollutants in metropolitan areas, United 

States, 2001-2004. Environmental Research. 110:294-301. 

Bell, M.L. and F. Dominici. 2008. Effect modification by community characteristics on the 

short-term effects of ozone exposure and mortality in 98 U.S. communities. American 

Journal of Epidemiology. 167:986-997. 

Bell, M.L.; A. McDermott; S.L. Zeger; J.M. Samet; F. Dominici. 2004. Ozone and short-term 

mortality in 95 U.S. urban communities, 1987-2000. JAMA. 292:2372-2378. 

Darrow, L.A.; M. Klein; J.A. Sarnat; J.A. Mulholland; M.J. Strickland; S.E. Sarnat, et al. 2011. 

The use of alternative pollutant metrics in time-series studies of ambient air pollution and 

respiratory emergency department visits. Journal of Exposure Science and Environmental 

Epidemiology. 21:10-19. 

Frey, C. and J. Samet. 2012. CASAC Review of the EPA’s Health Risk and Exposure Assessment 

for Ozone (First External Review Draft - Updated August 2012) and Welfare Risk and 

Exposure Assessment for Ozone (First External Review Draft - Updated August 2012). U.S. 

Environmental Protection Agency Science Advisory Board. EPA-CASAC-13-002. 

Frey, C. 2014. CASAC Review of the EPA’s Health Risk and Exposure Assessment for Ozone (Second 

External Review Draft – February, 2014). U.S. Environmental Protection Agency Science 

Advisory Board. EPA-CASAC-14-005. 

Gent, J.F.; E.W. Triche; T.R. Holford; K. Belanger; M.B. Bracken; W.S. Beckett, et al. 2003. 

Association of low-level ozone and fine particles with respiratory symptoms in children 

with asthma. Journal of the American Medical Association. 290(14):1859-1867. 

Ito, K.; G.D. Thurston and R.A. Silverman. 2007. Characterization of PM2.5, gaseous pollutants, 

and meteorological interactions in the context of time-series health effects models. 

Journal of Exposure Science and Environmental Epidemiology. 17(S2):S45-60. 

Jerrett, M.; R.T. Burnett; C.A. Pope, III; K. Ito; G. Thurston; D. Krewski; Y. Shi; E. Calle; and 

M. Thun. 2009. Long-term ozone exposure and mortality." New England Journal of 

Medicine. 360:1085-1095. 

Katsouyanni, K.; J.M. Samet; H.R. Anderson; R. Atkinson; A.L. Tertre; S. Medina, et al. 2009. 

Air Pollution and Health: A European and North American Approach (APHENA). Health 

Effects Institute. 

Lin, S.; E.M. Bell; W. Liu; R.J. Walker; N.K. Kim and S.A. Hwang. 2008a. Ambient ozone 

concentration and hospital admissions due to childhood respiratory diseases in New York 

State, 1991– 2001. Environmental Research. 108:42-47. 
7-89 

Lin, S; X. Liu; L.H. Le; S.A. Hwang. 2008. Chronic exposure to ambient ozone and asthma 

hospital admissions among children. Environmental Health Perspective. 116:1725-1730. 

Linn, W.S.; Y. Szlachcic; H. Gong, Jr.; P.L. Kinney and K.T. Berhane. 2000. Air pollution and 

daily hospital admissions in metropolitan Los Angeles. Environmental Health 

Perspective. 108(5):427-434. 

Medina-Ramon, M.; A. Zanobetti and J. Schwartz. 2006. The effect of ozone and PM10 on 

hospital admissions for pneumonia and chronic obstructive pulmonary disease: a national 

multicity study. American Journal of Epidemiology. 163(6):579-588. 

Meng, Y.Y.; R.P. Rull; M. Wilhelm; C. Lombardi; J. Balmes and B. Ritz. 2010. Outdoor air 

pollution and uncontrolled asthma in the San Joaquin Valley, California. Journal of 

Epidemiology Community Health. 64:142-147. 

Moore, K; R. Neugebauer; F. Lurmann; J. Hall; V. Brajer; S. Alcorn; I. Tager. 2008. Ambient 

ozone concentrations cause increased hospitalizations for asthma in children: an 18-year 

study in southern California. Environmental Health Perspective. 116:1063-1070. 

NRC. 2009. Science and Decisions, Advancing Risk Assessment. Committee on Improving Risk 

Analysis Approaches. Washington, DC: The National Academies Press, National 

Research Council. 

Sasser, E. 2014. Response to Comments Regarding the Potential Use of a Threshold Model in 

Estimating the Mortality Risks from Long-term Exposure to Ozone in the Health Risk and 

Exposure Assessment for Ozone, Second External Review Draft. Memorandum to Holly 

Stallworth, Designated Federal Officer, Clean Air Scientific Advisory Committee from 

EPA/OAQPS Health and Environmental Impacts Division. 

Silverman, R.A.; and K. Ito. 2010. Age-related association of fine particles and ozone with 

severe acute asthma in New York City. Journal of Allergy Clinical Immunology. 

125(2):367-373. 

Smith, R.L.; B. Xu and P. Switzer. 2009. Reassessing the relationship between ozone and shortterm mortality in U.S. urban communities. Inhalation Toxicology. 21:37-61. 

Strickland, M.J.; L.A. Darrow; M. Klein; W.D. Flanders; J.A. Sarnat; L.A. Waller, et al. 2010. 

Short-term associations between ambient air pollutants and pediatric asthma emergency 

department visits. American Journal of Respiratory Critical Care Medicine. 182:307-

316. 

Tolbert, P.E.; M. Klein; J.L. Peel; S.E. Sarnat and J.A. Sarnat. 2007. Multipollutant modeling 

issues in a study of ambient air quality and emergency department visits in Atlanta. 

Journal of Exposure Science and Environmental Epidemiology. 17(S2):S29-35. 

CDC. 2010. Table C1 Adult Self-Reported Current Asthma Prevalence Rate (Percent) and 

Prevalence (Number) by State or Territory. Centers for Disease Control and Prevention, 

Behavioral Risk Factor Surveillance System (BRFSS). Available at: 

<http://www.cdc.gov/asthma/brfss/2010/current/tableC1.htm>. 

U.S. EPA. 2001. Risk Assessment Guidance for Superfund. Vol. III, Part A. Process for 

Conducting Probabilistic Risk Assessment (RAGS 3A). Washington, DC: EPA. (EPA 

document number EPA 540-R-02-002; OSWER 9285.7-45; PB2002 963302). Available 

at: <http://www.epa.gov/oswer/riskassessment/rags3adt/index.htm)>. 

U.S. EPA. 2004. EPA’s Risk Assessment Process for Air Toxics: History and Overview. In: Air 

Toxics Risk Assessment Reference Library, Technical Resource Manual, Vol. 1, pp. 3-1 
7-90 

– 3-30. (EPA document number EPA-453-K-04-001A). Washington, DC: EPA. 

Available at: <http://www.epa.gov/ttn/fera/data/risk/vol_1/chapter_03.pdf)>. 

U.S. EPA. 2007. Ozone Health Risk Assessment for Selected Urban Areas. Research Triangle 

Park, NC: EPA Office of Air Quality Planning and Standards. (EPA document number 

EPA 452/R-07-009). Available at: 

<http://www.epa.gov/ttn/naaqs/standards/ozone/s_O3_cr.html>. 

U.S. EPA. 2009. Integrated Science Assessment for Particulate Matter: Final. Research Triangle 

Park, NC: U.S. Environmental Protection Agency. (EPA document number EPA/600/R08/139F). 

U.S. EPA. 2011. Ozone National Ambient Air Quality Standards: Scope and Methods Plan for 

Health Risk and Exposure Assessment. Research Triangle Park, NC: EPA. (EPA 

document number EPA-452/P-11-001). 

U.S. EPA. 2012. Health Risk and Exposure Assessment for Ozone. First External Review Draft. 

Research Triangle Park, NC: U.S. Environmental Protection Agency, Research Triangle 

Park, NC. (EPA document number EPA 452/P-12-001). 

U.S. EPA. 2013a. Integrated Science Assessment for Ozone and Related Photochemical 

Oxidants: Final. Research Triangle Park, NC: U.S. Environmental Protection Agency. 

(EPA document number EPA/600/R-10/076F). 

U.S. EPA. 2013b. Environmental Benefits Mapping Analysis Program (BenMAP v4.0). Posted 

January, 2013. < http://www.epa.gov/air/benmap/download.html />. 

WHO. 2008. Part 1: Guidance Document on Characterizing and Communicating Uncertainty in 

Exposure Assessment, Harmonization Project Document No. 6. Published under joint 

sponsorship of the World Health Organization, the International Labour Organization and 

the United Nations Environment Programme. WHO Press, World Health Organization, 

20 Avenue Appia, 1211 Geneva 27, Switzerland. 

Zanobetti, A; J. Schwartz. 2008. Mortality displacement in the association of ozone with 

mortality: an analysis of 48 cities in the United States. American Journal of Respiratory 

and Critical Care Medicine. 177:184-189.
8-1 

8 CHARACTERIZATION OF NATIONAL-SCALE MORTALITY RISK 

BASED ON EPIDEMIOLOGICAL STUDIES AND AN URBAN-SCALE 

REPRESENTATIVENESS ANALYSIS 

As described in Chapter 2, the O3 ISA (U.S. EPA, 2013) concluded that there is likely to 

be a causal relationship between short-term O3 exposure and all-cause mortality and that there is 

likely to be a causal relationship between long-term O3 exposure and respiratory effects, 

including respiratory mortality. In Chapter 7, we estimated epidemiological-based health risks 

associated with recent O3 concentrations and meeting the current and alternative O3 standards in 

12 selected urban study areas. In this chapter we estimate nationwide premature mortality 

attributable to recent short-term and long-term exposures to ambient O3 (Section 8.1) based on 

results from epidemiological studies; and assess the degree to which the selected urban study 

areas represent the full national distribution of risk-related attributes and air quality dynamics 

(Section 8.2). Compared with the urban-scale analysis in Chapter 7, this national-scale analysis 

incorporates fully, ambient O3 concentrations and population information across the entire 

continental U.S. however uses less geographic specificity in the concentration-response (C-R) 

functions that are used to calculate O3-attributable mortality. The national-scale analysis is 

therefore intended as a complement to the urban-scale analysis, providing both a broader 

assessment of O3-related health risks across the U.S. as well as an evaluation of how well the 

urban study areas examined in Chapter 7 represent the full distribution of O3-related health risks 

and air quality dynamics in the U.S. 

8.1 NATIONAL-SCALE ASSESSMENT OF MORTALITY RELATED TO OZONE 

EXPOSURE 

This section estimates the total annual deaths for 2007 populations associated with 

average 2006-2008 O3 levels across the continental U.S. We first describe the methods and 

inputs used to estimate O3-attributable risk across the continental U.S., including O3 exposure 

estimates, population and baseline mortality rate estimates, and epidemiological-based O3

mortality effect estimates. Results for the estimation of O3-attributable risk are then discussed in 

terms of the magnitude and percent of total mortality attributable to O3 exposure. We provide 

two analyses to give perspective on the confidence in the estimates of O3-related mortality: (1) 

risk estimated only within the urban areas for which particular O3 mortality effect estimates are 

available; and (2) the distribution of O3-related deaths across the range of observed 2006-2008 

average O3 concentrations fused with modeled 2007 concentrations. These results are then 

synthesized and compared with previous estimates of the burden of O3 exposure on mortality in 

the U.S. from the literature in a discussion section. 
8-2 

Figure 8-1. Conceptual Diagram for National-scale Mortality Risk Assessment. 

8.1.1 Methods 

This section describes the inputs and datasets used to conduct the national-scale 

assessment of O3-attributable risk. As shown in the conceptual diagram in Figure 8-1, we 

conduct this analysis using BenMAP 4.0, which uses projections of the size and geographic 

distribution of the potentially exposed population along with estimates of the ambient O3

concentrations to estimate O3-attributable health risks. In general, this analysis uses the same 

analytical structure and many of the same inputs as are used in the epidemiology-based 

assessment of O3-attributable risk in the selected urban study areas in Chapter 7. We refer back 

to Chapter 7 for details on these shared inputs, and describe where the urban-scale and nationalscale analyses use divergent methods. 

Concentration-Response Functions

Population Information

National ambient ozone 

12 km x 12km

gridded spatial field 

for recent year

Air Quality Inputs (Chapter 4)

Identify 

national scale

epidemiological 

studies from the ISA

Identify 

Relative Risk

(RR) or slope 

coefficients (ß)

Convert 

RR to ß

Nationwide set of city

specific C-R functions 

Identify 

functional form

Identify appropriate 

modeling period

Daily county-specific 

baseline health incidence

Population allocated 

to 12 km x12 km grid

Compute gridded ozone-attributable 

mortality incidence for time period 

matching C-R function season 

BenMAP

County and national level 

estimates of % of total mortality 

attributable to ozone

County and national level

estimates of burden of premature 

mortality attributable to ozone
8-3 

8.1.1.1 Ambient ozone concentrations 

Air quality inputs to this analysis are described in detail in Chapter 4. In contrast to the 

urban-scale analysis in Chapter 7, the national-scale analysis employs a data fusion approach that 

takes advantage of the accuracy of monitor observations and the comprehensive spatial 

information of the CMAQ modeling system to create national-scale “fused” spatial surfaces of 

seasonal average O3. Measured O3 concentrations from 2006-2008 were fused with modeled 

concentrations from a 2007 CMAQ model simulation, run for a 12 km domain covering the 

contiguous U.S. The spatial surfaces are created using EPA’s Downscaler software (Berrocal et 

al., 2012).1 More details on the ambient measurements, the 2007 CMAQ model simulation, the 

Downscaler fusion technique, and a technical justification for changing from eVNA to 

Downscaler can be found in Chapter 4. 

Three “fused” spatial surfaces were created for: (1) the May-September mean of the daily 

maximum 8-hour (8-hr) average concentration (consistent with the metric used by Smith et al. 

2009); (2) the June-August mean of the daily 8-hr average concentration occurring between 

10am to 6pm (consistent with the metric used by Zanobetti and Schwartz, 2008); and (3) the 

April-September mean of the daily maximum 1-hour (1-hr) concentration (consistent with the 

metric use by Jerrett et al., 2009) O3 concentrations across the continental U.S. These fused 

spatial surfaces each represent one seasonal average across 2006-2008, rather than three separate 

years of concentrations. Section 4.3.2 presents maps, distributions, and statistical 

characterizations of these O3 concentrations metrics across the U.S., including how they compare 

to 2006-2008 design values. 

8.1.1.2 Concentration-response functions 

While Chapter 7 assessed both mortality and morbidity risks associated with O3

concentrations, due to limitations in information available for baseline morbidity incidence rates, 

the national scale assessment focuses on mortality risks only. To quantify the impact of O3

concentrations on mortality, we apply effect estimates drawn from two major short-term 

epidemiological studies and one long-term epidemiological study. These studies are consistent 

with those used in the analysis of O3-related risk in selected urban study areas (Section 7.2) and 

those mortality endpoints concluded to have a causal or suggestive causal relationship with O3

exposure by the 2013 O3 ISA (U.S. EPA, 2013). As described in detail in Section 7.2, we 

selected C-R functions by applying a number of criteria including: (1) the study was peerreviewed, evaluated in the O3 ISA, and judged adequate by EPA staff for purposes of inclusion 

 

1

 In the first draft of the HREA, the spatial surfaces were created using the enhanced Voronoi Neighbor Averaging 

(eVNA) technique (Timin et al., 2010) and using the EPA’s Model Attainment Test Software (MATS; Abt 

Associates, 2010b). 
8-4 

in the risk assessment; (2) Preference was given for multicity studies because they typically have 

greater statistical power and reflect patterns of O3 related health effects over a range of urban 

areas (and regions) which can display variability in key risk-related factors such as exposure 

measurement error; (3) The study design is considered robust and scientifically defensible, 

particularly in relation to methods for covariate adjustment, including treatment of confounders, 

as well as treatment of effect modifiers; and (4) The study is not superseded by another study 

(e.g., if a later study is an extension or replication of a former study, the later study would 

effectively replace the former study), unless the earlier study has characteristics that are clearly 

preferable (e.g., inclusion of copollutants models, or use of a peak exposure metric of interest). 

For short-term mortality, we use city-specific and national average risk estimates drawn 

from the Smith et al. (2009) study of O3 and mortality in 98 U.S. urban communities between 

1987 and 2000 as our main results, and the Zanobetti and Schwartz (2008) study of O3 and 

mortality in 48 U.S. cities between 1989 and 2000 as a sensitivity analysis, consistent with the 

urban study area analysis performed in Chapter 7. The city-specific effect estimates obtained 

from both studies are provided in Appendix 8A. 

Smith et al. (2009) found that the average non-accidental mortality increase across all 98 

urban areas studied was 0.32% ± 0.08 (95% posterior interval [PI], 0.41%-0.86%) for a 10 ppb 

increase in the daily maximum 8-hr average O3 concentration, based on April to October O3

concentrations. Because the national-scale analysis requires a single modeling period definition 

but some monitors only collect data from May to September, the corresponding city-specific 

effect estimates are applied to each day from May to September in BenMAP using the May to 

September mean of the daily maximum 8-hr average O3 concentration based on 2006-2008 

observed concentrations fused with 2007 modeled concentrations. The length of the O3 season 

can affect the magnitude of mortality effect estimates – a longer season may yield higher effect 

estimates per unit O3 concentration since O3 concentrations over a longer season may be lower 

than the O3 concentrations that occur over the warmest months only. Conversely, if the longer 

period captures periods of lower O3-related mortality incidence, the effect estimates may be 

lower than effect estimates for the warmest months only. Our application of the Smith et al. 

(2009) April to October effect estimates to the May through September O3 concentrations likely 

introduces some bias in the results, but it is unclear in which direction. 

Zanobetti and Schwartz (2008) found that the average total mortality increase across all 

48 cities studied was 0.53% (95% confidence interval, 0.28%-0.77%) for a 10 ppb increase in the 

June to August mean of the daily 8-hr average concentration occurring between 10am to 6pm, 

using a 0-3 day lag. We apply the city-specific effect estimates that correspond to this national 

average effect estimate each day from June to August in BenMAP using the June to August, 

means of the daily 8-hr average O3 concentration occurring between 10am to 6pm based on 
8-5 

2006-2008 observed concentrations fused with 2007 modeled concentrations. Consistent with 

Chapter 7, these results are presented as a sensitivity analysis. 

As in Chapter 7, we use city-specific risk estimates from the short-term epidemiology 

studies, but apply them here only to the counties that were included in the epidemiology studies 

rather than to the entire core-based statistical area (CBSA). Chapter 7 estimated risk across entire 

CBSAs to more completely capture expected O3 changes across broader areas and avoid bias 

resulting from including only those areas where O3 is expected to increase under alternative 

standards. The inclusion of the entire CBSA in that analysis required the application of a single 

effect estimate to the entire CBSA. However, the national-scale assessment is a gridded analysis, 

which allows greater spatial resolution in the application of effect estimates. In addition, eight 

CBSAs nationwide included multiple cities defined separately by Smith et al. (2009), some of 

which showed considerable heterogeneity in effect estimates within the same CBSA. 

Heterogeneity among effect estimates within a single CBSA implies that effect estimates from 

one county may not be accurate representations of effect estimates in nearby 

counties. However, since city-specific effect estimates often have low power due to small 

population size, we are unable to draw a strong conclusion regarding how well one county's 

effect estimates represents those in nearby counties. For this national-scale assessment, we 

apply effect estimates from each city as defined in the epidemiology studies to retain the full set 

of information available from those studies. In addition, for counties not included by the 

epidemiology studies, we apply the average effect estimate derived from all the urban areas 

included in each of the studies (“national average”) as it takes advantage of a wider and more 

diverse population. 

Since both national average estimates from these studies are based on urban areas only, 

we have higher confidence in their application to other U.S. urban areas than to rural areas. To 

demonstrate the magnitude of the results for which we have the highest confidence, we present 

the percentage of estimated deaths occurring within the urban areas included in the 

epidemiological studies and within all urban areas across the U.S. Lower confidence in the 

results for rural areas does not indicate that the mortality risk among populations living in such 

areas is unaffected by O3 pollution. Rather, the level of understanding for the O3-mortality 

relationship in these areas is simply lower due to a lack of available epidemiological data at these 

levels. We also examine the effect of varying the effect estimate applied between the cities 

included by the epidemiology studies in a sensitivity analysis. 

We quantify long-term O3-related respiratory mortality in this Health Risk and Exposure 

Assessment (HREA) because the O3 ISA concluded that the evidence supports a likely to be 

causal relationship between long-term O3 exposure and respiratory effects, including respiratory 

morbidity and respiratory-related mortality (U.S. EPA, 2013). As detailed in Chapter 7, we 
8-6 

quantify long-term O3-related mortality using the respiratory mortality effect estimates from the 

Jerrett et al. (2009) two-pollutant model that controlled for PM2.5 concentrations, applied to each 

grid cell across the entire United States. This model found that a 10 ppb increase in the AprilSeptember mean of the daily maximum 1-hr O3 concentration was associated with a 4% (95% 

confidence interval, 1.0%-6.7%) increase in respiratory mortality. 

8.1.1.3 Demographic inputs 

This analysis uses the same baseline mortality rates and population estimates as were 

used in the urban study area analysis in Chapter 7. We derive baseline incidence rates for 

mortality by age, cause, and county from the CDC Wonder database (CDC, 2004-2006). As this 

database only provides baseline incidence rates in 5-year increments, we use data for the year 

2005, the closest year to the analysis year 2007 used for the population and air quality modeling. 

We use 2007 population because it matches both the year of the emissions inventory and 

meteorology used for the air quality modeling. 

The starting point for estimating the size and demographics of the potentially exposed 

population is the 2010 census-block level population, which BenMAP aggregates up to the same 

grid resolution as the air quality model. BenMAP back-casts this 2010 population to the analysis 

year of 2007 using county-level growth factors based on economic projections (Woods and 

Poole Inc., 2012). 

8.1.2 Results 

Table 8-1 summarizes the estimated O3-related premature mortality associated with 2006-

2008 average O3 concentrations under various assumptions for the health impact function. 

Applying Smith et al. (2009) effect estimates for May-September, we estimate 15,000 (95% CI, 

1,400-28,000) premature O3-related non-accidental deaths annually for 2007. As a sensitivity 

analysis, we apply Zanobetti and Schwartz (2008) effect estimates for June-August, finding 

16,000 (95% CI, 6,000-25,000) premature O3-related all-cause deaths annually for 2007. Figure 

8-2 through Figure 8-4 show that estimated O3-related mortality is most concentrated in highly 

populated counties or those counties with urban areas found to have high effect estimates by 

Smith et al. (2009) or Zanobetti and Schwartz (2008). For the application of Jerrett et al. (2009) 

national average effect estimate for April-September, we estimate 45,000 (95% CI, 17,000-

70,000) premature O3-related respiratory deaths among adults age 30 and older.

Because the epidemiological studies included only selected urban areas, we are more 

confident in the magnitude of the estimated O3-related deaths occurring within those urban areas. 

As shown in Table 8-1, approximately 43% of the O3-related deaths estimated using Smith et al. 

(2009) effect estimates occur in the 98 urban areas included in that study, and 30% of the O3-
8-7 

related deaths estimated using Zanobetti and Schwartz (2008) effect estimates occur in the 48 

urban areas included in that study. The cities included in each epidemiological study are listed in 

Appendix 8A. We are also more confident in extrapolating the national average effect estimates 

to other urban areas than we are to rural areas, as the national average estimates are based on all 

urban areas included by the study. To estimate the percentage of total O3-attributable deaths 

occurring within all urban areas across the continental U.S., we sum the results for the 12 km 

grid cells that have a total population greater than 12,000 (approximately equal to the 95th

percentile of grid cell populations across the continental U.S.). The percentage of O3-attributable 

deaths occurring within urban areas defined in this way is 65% for results based on Smith et al. 

(2009) effect estimates and 64% for results based on Zanobetti and Schwartz (2008) effect 

estimates. While our confidence is lower when the national average effect estimates are 

extrapolated to rural areas, less certainty in the magnitude of O3-related deaths in rural areas does 

not imply that O3 has no effect on health in these areas. 

Table 8-1. Estimated Annual O3-related Premature Mortality in 2007 Associated with 

2006-2008 Average O3 Concentrations (95 percent confidence interval). 

1 City-specific effect estimates are applied to the grid cells lying within the cities defined in the epidemiological 

studies. Average effect estimates across all cities included in the epidemiological studies (national average) are 

applied to all other grid cells. For the application of Smith et al. (2009) effect estimates, city-specific effect estimates 

were applied to 2,227 grid cells and the national average to 44,064 grid cells. For the application of Zanobetti and 

Schwartz (2008) effect estimates, city-specific effect estimates were applied to 925 grid cells and the national 

average to 45,366 grid cells. 

2 National average effect estimates are based on the average of all cities included in the epidemiological studies 

applied to all 12km grid cells nationally. 

3 O3-attributable deaths are summed in each city within BenMAP using area weights based on a shapefile definition 

of the counties included in each city. Summed city-specific results are then divided by the total U.S. O3-attributable 

deaths to generate the percentage occurring within the cities included by Smith et al. (2009) and Zanobetti and 

Schwartz (2008). 

Source of Risk Estimate and Modeling 

Period 

Exposure 

Duration 

Study 

Subject 

Ages 

Annual O3-related Premature 

Mortality 

City-specific 

Effect 

Estimates1

National 

Average Effect 

Estimate2

Smith et al. (2009), May-Sep Short-term >0 15,000 15,000 

(95% confidence interval) (1,400-28,000) (7,100-22,000) 

% occurring within the 98 cities3 43% 

Zanobetti & Schwartz (2008), Jun-Aug Short-term >0 16,000 15,000 

 (95% confidence interval) (5,900-25,000) (8,300-22,000) 

% occurring within the 48 cities3 30% 

Jerrett et al. (2009), Apr-Sep Long-term ≥30 years - 45,000 

(95% confidence interval) (16,000-70,000) 
8-8 

Table 8-1 also shows O3-related deaths estimated by applying the national average risk 

estimate from the epidemiological studies to all grid cells in the U.S. As discussed in detail in 

Section 7.4.1, applying city-specific effect estimates accounts for heterogeneity between cities 

due to differences in population characteristics, potential confounding, potential for the presence 

of averting behavior, and variation in sample sizes which can affect stability of effect estimates. 

By contrast, the national average effect estimate does not distinguish differential effects between 

cities but has the advantage of a substantially larger sample size that includes a wider range of 

populations, confounding factors, and behaviors. Compared with applying city-specific effect 

estimates to the grid cells corresponding to each urban area, using the national average effect 

estimate for all grid cells yields equivalent central estimates. However, applying the national 

average also results in tighter confidence intervals since the national average effect estimates had 

higher statistical power and thus tighter confidence bounds compared with the effect estimates 

for individual cities. 

Table 8-2 shows the mean, median, 2.5th percentile and 97.5th percentile of the estimated 

percentage of mortality attributable to ambient O3 across all counties in the U.S. Using Smith et 

al. (2009) effect estimates, O3-attributable mortality contributes an average of 1.5% (95% 

confidence interval, 1.1%-1.8%) to county-level May-September non-accidental mortality (all 

ages) and 0.6% (0.4%-0.7%) to all year all-cause mortality (all ages). For results using Zanobetti 

and Schwartz (2008) effect estimates, O3-attributable mortality contributes an average of 2.5% 

(95% confidence interval, 1.7%-3.0%) to county-level June-August all-cause mortality (all ages) 

and 0.6% (0.4%-0.8%) to all year all-cause mortality (all ages). For the results using Jerrett et al. 

(2009) effect estimates, O3-attributable mortality contributes an average of 18.5% (95% 

confidence interval, 15.2%-21.5%) to county-level April-September adult (age 30+) respiratory 

mortality and 1.9% (1.3%-2.6%) to all year all-cause mortality (all ages). Figure 8-5 through

Figure 8-7 show that the counties with the highest percentage of mortality attributable to O3 are 

typically those with the highest O3 levels.
8-9 

Table 8-2. Mean, Median, 2.5th Percentile, and 97.5th Percentile of the Estimated 

Percentage of Mortality Attributable to Ambient O3 for all 3,109 Counties in the 

Continental U.S. 

Source of Risk Estimate, Modeling 

Period, and Mortality Endpoints1

Total 

Mortality 

(2005) 

Percentage of Total Mortality Attributable to O3

Mean 

(%) 

Median 

(%) 

2.5th 

Percentile 

(%)

97.5th

Percentile 

(%) 

Smith et al. (2009), May-Sep 

Non-accidental mortality, all ages 960,000 1.5 1.5 1.1 1.8 

All-cause mortality, all ages 1,000,000 1.4 1.4 1.0 1.7 

All-cause mortality, all ages, all year 2,500,000 0.6 0.6 0.4 0.7 

Zanobetti & Schwartz (2008), Jun-Aug 

All-cause mortality, all ages 620,000 2.5 2.5 1.7 3.0 

All-cause mortality, all ages, all year 2,500,000 0.6 0.6 0.4 0.8 

Jerrett et al. (2009), Apr-Sep 

Respiratory mortality, ages 30+ 240,000 18.5 18.7 15.2 21.5 

All-cause mortality, all ages 1,200,000 3.8 3.7 2.6 5.2 

All-cause mortality, all ages, all year 2,500,000 1.9 1.9 1.3 2.6 

2 For the mortality endpoints matching the epidemiology studies as a percentage of incidence of the same endpoint 

for the same seasonal definition, and as a percentage of all-cause mortality for all age groups (both seasonal and all 

year). 

 
8-10 

Figure 8-2. Estimated Annual non-Accidental Premature Deaths (individuals) in 2007 

Associated with Average 2006-2008 May-September Means of the Daily Maximum 8-hr 

Average O3 Levels by U.S. County using Smith et al. (2009) Effect Estimates. 

Figure 8-3. Estimated Annual all-Cause Premature Deaths (individuals) in 2007 Associated 

with Average 2006-2008 June-August Means of the Daily 8-hr Average (10am-6pm) O3

Levels by U.S. County using Zanobetti and Schwartz (2008) Effect Estimates. 
8-11 

Figure 8-4. Estimated Annual Adult (age 30+) Respiratory Premature Deaths (individuals) 

in 2007 Associated with Average 2006-2008 April-September Means of the Daily Maximum 

1-hr O3 Levels by U.S. County using Jerrett et al. (2009) Effect Estimates 

Figure 8-5. Estimated Percentage of May-September Total non-Accidental Mortality (all 

ages) Attributable to 2006-2008 average O3 Levels by U.S. County using Smith et al. (2009) 

Effect Estimates. 
8-12 

Figure 8-6. Estimated Percentage of June-August Total all-Cause Mortality (all ages) 

Attributable to 2006-2008 Average O3 Levels by U.S. County using Zanobetti and Schwartz 

(2008) Effect Estimates. 

Figure 8-7. Estimated Percentage of April-September Respiratory Mortality among Adults 

Age 30+ Attributable to 2006-2008 Average O3 Levels by U.S. County using Jerrett et al. 

(2009) Effect Estimates. 
8-13 

Figure 8-8. Cumulative Distribution of County-level Percentage of all-cause, all-year, and 

all-age Mortality Attributable to 2006-2008 Average O3 for the U.S. 

Figure 8-8 displays the cumulative distribution of the percent of county-level all-cause, 

all-age, and all-year mortality attributable to ambient O3 using effect estimates from all three 

epidemiological studies.2

 For the results based on Smith et al. (2009) and Zanobetti and Schwartz 

(2008) effect estimates, 0.8% of all-cause, all-age, and all-year mortality is attributable to O3 for 

approximately 99% of U.S. counties. For the results based on Jerrett et al. (2009) effect 

estimates, 2.8% of all-cause, all-age, and all-year mortality is attributable to O3 for 

approximately 99% of U.S. counties. 

Figure 8-9 shows the cumulative distribution of the county-level percent of total O3-

related deaths by O3 concentration. The mortality results based on Smith et al. (2009) C-R 

functions are compared with the May-September mean of the daily maximum 8-hr average O3

concentration, those based on Zanobetti and Schwartz (2008) C-R functions are compared with 

the June-August mean of the 8-hr average O3 concentration from 10am to 6pm, and those based 

 

2

 Estimated O3-attributable deaths are based on the mortality cause, age group, and season inherent to the 

epidemiological study upon which it is based (May-September non-accidental mortality for all ages for results 

based on Smith et al. (2009) effect estimates, June-August all-cause mortality for all ages for results based on 

Zanobetti and Schwartz (2008) effect estimates, and April-September respiratory mortality for ages 30+ for results 

based on Jerrett et al. (2009) effect estimates). 
8-14 

on Jerrett et al. (2009) C-R functions are compared with the April-September mean of the daily 

maximum 1-hr O3 concentration, consistent with the O3 concentration metrics used in each 

study. The mortality results based on Zanobetti and Schwartz (2008) effect estimates are shifted 

to the right of the mortality results based on the Smith et al. (2009) C-R functions because the 

seasonal averaging time for the results based on Zanobetti and Schwartz (2008) is limited to the 

summer months when O3 tends to be highest. Similarly, the mortality results based on Jerrett et 

al. (2009) effect estimates are shifted to the right of the mortality results based on Zanobetti and 

Schwartz (2008) and Smith et al. (2009) because Jerrett et al. (2009) results use the seasonal 

mean of the daily maximum 1-hr, which tends to be higher than the seasonal mean of the daily 

maximum 8-hr and seasonal mean of the daily 8-hr average metrics (see Figure 4-17). For all 

three epidemiology studies, we find that 90-95% of O3-related deaths occur in locations where 

the May to September mean of the daily maximum 8-hr average concentration, June to August 

mean of the daily 8-hr average (10am-6pm), or April to September mean of the daily maximum 

1-hr O3 concentrations are greater than 40 ppb. A seasonal mean concentration of 40 ppb 

corresponds to 2006-2008 design values ranging from approximately 50 to 90 ppb, depending on 

the seasonal mean concentration metric (see Figure 4-18). 

Figure 8-9. Cumulative Percentage of Total O3 deaths by Baseline O3 Concentration. 

Ozone Concentrations are Reported as May-September Mean of the Daily Maximum 8-hr 

Average Concentration for Results based on Smith et al. (2009) Effect Estimates, JuneAugust Mean of the Daily 8-hr Average (10am to 6pm) for Results based on Zanobetti and 

Schwartz (2008) Effect Estimates, and April-September Mean of the Daily Maximum 1-hr 

Concentration for Results based on Jerrett et al. (2009) Effect Estimates. 
8-15 

8.1.3 Sensitivity Analysis 

For the results presented above, the national average effect estimate for results based on 

Smith et al. (2009) and Zanobetti and Schwartz (2008) was applied to all grid cells between the 

cities included in the studies. However, O3-mortality effect estimates have been shown to exhibit 

significant regional variability across the U.S. (e.g. Smith et al. 2009). Smith et al. (2009) found 

that using the national average effect estimate may overestimate risk in cities that have low effect 

estimates, including Los Angeles and Denver, but may underestimate risk in cities that have high 

effect estimates, including New York City and Chicago. We conduct two sensitivity analyses 

aimed at characterizing the sensitivity of estimated O3-attributable premature deaths to the use of 

national average effect estimates between the cities that were included in these two studies. 

First, we examine the sensitivity of estimated O3-attributable premature deaths to the 

application of the 5th highest and 5th lowest effect estimates of all the cities included in the Smith 

et al. (2009) and Zanobetti and Schwartz (2008) studies to the grid cells between the cities 

included in these studies (Table 8-3). As in the main results, city-specific effect estimates are 

applied to the grid cells in which the cities lie. Applying the 5th highest effect estimate from Las 

Vegas to the grid cells between the cities included by Smith et al. (2009) yields a 36% lower 

estimate of O3-attributable deaths as compared with the main results. Applying the 5th lowest 

effect estimate from Dallas/Ft. Worth yields a 42% higher estimate of O3-attributable deaths as 

compared with the main results. Applying the 5th lowest effect estimate from Los Angeles to the 

grid cells between the cities included by Zanobetti and Schwartz (2008) yields a 37% lower 

estimate of O3-attributable deaths as compared with the main results. Applying the 5th highest 

effect estimate from Columbus, OH, yields a 30% higher estimate of O3-attributable deaths as 

compared with the main results. 

Second, we examine the sensitivity of estimated O3-attributable premature deaths to the 

application of Smith et al. (2009) Bayesian-shrunken city-specific estimates using regional 

average priors rather than the national average prior (Table 8-4). For grid cells between the cities 

included by Smith et al. (2009), we apply the regional average effect estimate, rather than the 

national average effect estimate as in the main results. Regional definitions are shown in Figure 

8-10. Estimated O3-attributable deaths using the regional prior city-specific effect estimates and 

the regional average effect estimates between the 98 cities included by Smith et al. (2009) are 

approximately 20% larger than the main results, with 38% of estimated deaths occurring in the 

98 cities rather than 43%. The 95% confidence interval for the results using the regional prior 

spans zero, whereas the 95% confidence interval for the results using the national prior does not. 

Since the regional average effect estimates are all based on fewer data points (in some regions, 

the regional average is based on only seven cities; see Appendix 8A) than is the national average, 

the confidence interval for each regional average effect estimate is large and sometimes spans 
8-16 

zero. The large confidence intervals for the regional average effect estimates drive the 

confidence interval that spans zero for O3-attributable mortality estimated using regional prior 

effect estimates. Confidence intervals that span zero do not imply that higher O3 is associated 

with decreased mortality, as there is no biologically plausible mechanism for such an effect, and 

in no case do we see a significant negative central estimate. Rather, confidence intervals 

spanning zero indicate a lack of statistical power to precisely determine the magnitude of an 

effect. 

Table 8-3. Sensitivity of Estimated O3-attributable Premature Deaths to the Application of 

the 5th lowest and 5th highest City-specific Risk estimates found by Smith et al. (2009) and 

Zanobetti and Schwartz (2008) to the Grid Cells that do not correspond to the Cities 

Included in Those Studies. 

Source of Risk Estimate and 

Sensitivity Investigated Beta Used and City 

O3-attributable 

Mortality 

(95% confidence 

interval) 

Percent Change 

from Main 

Results 

Smith et al. (2009), May-Sep 

5th lowest beta 0.00014 

Las Vegas, NV 

9,600 

(-20,000 – 38,000) 

-36% 

5th highest city beta 0.000538 

Dallas/Ft. Worth, TX 

21,000 

(-1000 – 43,000) 

+42% 

Zanobetti & Schwartz (2008), 

Jun-Aug 

 

5th lowest city beta 0.000274 

Los Angeles, CA 

9,800 

(-3,700 – 23,000) 

-37% 

5th highest city beta 0.000739 

Columbus, OH 

20,000 

(100 – 40,000) 

+30% 

Table 8-4. Sensitivity of Estimated O3-attributable Premature Deaths to the Application of 

Smith et al. (2009) Regional-prior Bayes-shrunken City-specific and Regional-average 

Effect Estimates, as Compared with the National-prior Bayes-shrunken City-specific and 

National-average Effect Estimates as Done for the Main Results. 

Risk Estimate O3-attributable Premature Deaths

Percent O3-attributable 

Deaths in 98 cities

City-specific, national-prior 

with national-average 

15,000 

(1,400 – 28,000) 43% 

City-specific, regional-prior 

with regional-average 

18,000 

(-2,000 – 24,000) 38% 
8-17 

Figure 8-10. Seven Regions Used in the Sensitivity Analysis based on the Smith et al. 

(2009) Regional-prior Bayes-shrunken City-specific and Regional Average Effect Estimates 

(Source: Samet et al., 2000). 

Figure 8-11 shows estimated O3-attributable deaths by region using the national average 

prior compared with using the regional average priors from Smith et al. (2009). Results generally 

follow conclusions made by Smith et al. (2009) based on the magnitude of the regional effect 

estimates. For example, using the national average effect estimate may substantially 

underestimate O3-attributable deaths in the North East and Industrial Midwest where regional 

effect estimates are large. Using the national average effect estimate may also overestimate O3-

attributable deaths in the Upper Midwest, Southern California, and South West, which were 

found to have small effect estimates. However, these three regions have very large confidence 

intervals which all span zero, since these regional averages are based on few cities (7, 7, and 9, 

respectively, compared with 26 in the South East, 19 in Industrial Midwest, 16 in North East, and 

12 in North West; see Appendix 8A). 
8-18 

Figure 8-11. Ozone-attributable Premature Deaths by Region as Calculated by Applying 

Smith et al. (2009) Regional-prior Bayes-shrunken and Regional-average Effect Estimates, 

as Compared with the National-prior Bayes-shrunken and National-average Effect 

Estimates as Done for the Main Results. 

As in Chapter 7, we also examine the sensitivity of respiratory mortality associated with 

the six month mean of the daily maximum 1-hr O3 concentrations to possible low-concentration 

thresholds. The Jerrett et al. (2009) mortality model that included a low-concentration threshold 

at 56 ppb had the lowest log likelihood value for all models examined. However, it is unclear 

whether the 56 ppb threshold model better predicts respiratory mortality compared with a linear 

model for the Jerrett et al. (2009) data. Using different but valid statistical tests produced 

different conclusions about the strength of the threshold model compared with the linear model. 

A less stringent statistical test suggested the 56 ppb threshold model to have an improved model 

fit compared to that of the linear model, but as indicated by the confidence interval, valid 

threshold levels could range anywhere from 0 to 60 ppb. None of the threshold models produce 

better predictions than the linear model when a more stringent statistical test was used. 

We examine as a sensitivity analysis the influence of various low-concentration 

thresholds on estimated O3-related premature respiratory deaths calculated using the Jerrett et al. 

(2009) effect estimates. We examine a range of 40 ppb to 60 ppb thresholds in 5 ppb increments, 

including also a threshold equal to 56 ppb, which had the lowest log likelihood value for all 

models examined. Because the threshold model effect estimates given by Jerrett et al. (2009) did 

not control for PM2.5 but our main results use the 2-pollutant model which did control for PM2.5, 

we also include as a sensitivity a single pollutant no threshold model to be comparable with the 

‐5000 0 5000 10000 15000

Industrial Midwest

North East

North West

South East

South West

Southern California

Upper Midwest

Ozone‐attributable premature deaths

national prior regional prior
8-19 

single pollutant threshold models. In addition, the two-pollutant model used for the main results 

was based on 86 cities, while the single pollutant models were based on 96 cities. Therefore, for 

comparability to the main results, we also include as a sensitivity a single pollutant no threshold 

model based on 86 cities. 

When no low-concentration threshold is applied (as in the main results), we estimate 

31,000 (95% confidence interval, 10,000 – 51,000) O3-attributable premature deaths using the 86 

city O3-only model and 34,000 (13,000-53,000) using the 96 city O3-only model (Table 8-5). 

These results are 30% and 25% fewer than the 45,000 (17,000 – 70,000) O3-attributable 

premature deaths calculated using the two-pollutant model for 86 cities (used for the main 

results). For the results based on the O3-only models with thresholds ranging from 40-60 ppb, we 

estimate 71-98% fewer O3-attributable deaths compared with results based on the O3-only no 

threshold model of 96 cities and 78-99% fewer compared with the main results. For a 56 ppb 

threshold, which had the lowest log likelihood value for all models examined, we estimate 1,600 

(710-2,400) O3-attributable premature deaths, 95% fewer compared with results based on the O3-

only no threshold model of 96 cities and 97% fewer than the main results. 

Table 8-5. Sensitivity of Estimated O3-attributable Premature Deaths to the Application of 

Jerrett et al. (2009) Effect Estimates with and without a Low Concentration Threshold. 

Model Threshold Beta 

O3-attributable 

Premature Deaths 

(95% Confidence 

Interval) 

Percent 

Change 

from Main 

Results 

Percent 

Change from 

O3 only, 96 

cities, No 

Threshold 

Model 

Two-pollutant 

model, 86 cities 0 ppb 0.0039221 45,000 (16,000 – 70,000) n/a +33% 

O3-only model, 

86 cities 0 ppb 0.0026642 31,000 

(9,500 – 51,000) -30% -6% 

O3-only model, 

96 cities 

0 ppb 0.00286 34,000 

(13,000 – 53,000) -25% n/a 

40 ppb 0.00312 9,800 

(4,000 – 16,000) -78% -71% 

45 ppb 0.00336 7,000 

(2,900 – 11,000) -84% -79% 

50 ppb 0.00356 3,900 

(1,700 – 6,200) -91% -88% 

55 ppb 0.00417 1,900 

(840 – 2,900) -96% -94% 

56 ppb 0.00432 1,600 

(710 – 2,400) -97% -95% 

60 ppb 0.00402 620 

(210 – 1,000) -99% -98% 
8-20 

8.1.4 Discussion 

We estimated the total all-cause deaths associated with short-term exposure to recent O3

levels across the continental U.S., using average 2006-2008 observations from the O3 monitoring 

network fused with a 2007 CMAQ simulation and city-specific O3-mortality effect estimates 

from two short-term epidemiology studies. Applying Smith et al. (2009) effect estimates for 

May-September, we estimate 15,000 (95% CI, 1,400-28,000) premature O3-related nonaccidental deaths (all ages) annually for 2007. Using Smith et al. (2009) effect estimates, O3-

attributable mortality contributes an average of 1.5% (95% confidence interval, 1.1%-1.8%) to 

county-level May-September non-accidental mortality (all ages) and 0.6% (0.4%-0.7%) to all 

year all-cause mortality (all ages). As a sensitivity, we apply Zanobetti and Schwartz (2008) 

effect estimates for June-August, finding 16,000 (95% CI, 6,000-25,000) premature O3-related 

all-cause deaths (all ages) annually for 2007. For results using Zanobetti and Schwartz (2008) 

effect estimates, O3-attributable mortality contributes an average of 2.5% (95% confidence 

interval, 1.7%-3.0%) to county-level June-August all-cause mortality (all ages) and 0.6% (0.4%-

0.8%) to all year all-cause mortality (all ages). For the application of Jerrett et al. (2009) effect 

estimates for April-September, we estimate 45,000 (95% CI, 17,000-70,000) premature O3-

related adult (age 30 and older) respiratory deaths. For the results using Jerrett et al. (2009) effect 

estimates, O3-attributable mortality contributes an average of 18.5% (95% confidence interval, 

15.2%-21.5%) to county-level April-September adult (age 30+) respiratory mortality and 1.9% 

(1.3%-2.6%) to all year all-cause mortality (all ages). For all three epidemiology studies, we find 

that 90-95% of O3-related deaths occur in locations where the May to September means of the 

daily maximum 8-hr average concentration, June to August means of the daily 8-hr average 

(10am-6pm), or April to September means of the daily maximum 1-hr O3 concentrations are 

greater than 40 ppb. A seasonal mean concentration of 40 ppb corresponds to 2006-2008 design 

values ranging from approximately 50 to 90 ppb, depending on the seasonal mean concentration 

metric. 

A previous analysis estimated that short-term O3 exposure was associated with 4,700 

(95% CI, 1,800-7,500) premature deaths nationwide annually, based on 2005 O3 concentrations 

and Bell et al. (2004) national average effect estimates (Fann et al., 2012). The results estimated 

here are higher, resulting mainly from two important differences. First, Fann et al. (2012) 

estimated risk only above North American background, simulated O3 concentrations in the 

absence of North American anthropogenic emissions, which was set to 22 ppb in the east and 30 

ppb in the west. Fann et al. (2012) also used a national average mortality effect estimate for daily 

maximum 8-hr average O3 during the warm season only, calculated using ratios of 24-hr mean 

concentrations to daily maximum 8-hr average concentrations (see Abt Associates 2010). The 

Smith et al. (2009) national average beta used here, 0.000322, is based on April-October O3 data 
8-21 

and is approximately 23% larger than that used by Fann et al. (2012), 0.000261. Because the risk 

modeling period (and the seasonal definition for the seasonal mean of the daily maximum 8-hr 

average concentration) was May to September for both studies, the higher beta used here yields a 

larger O3 mortality estimate. These two differences in methods explain the larger O3 mortality 

estimates of this analysis compared with the previous estimate by Fann et al. (2012). 

Estimated O3-attributable premature deaths based on Jerrett et al. (2009) effect estimates 

are approximately three times larger than results based on Smith et al. (2009) and Zanobetti and 

Schwartz (2008) effect estimates. The mean estimated county-level percent of all-cause, all-year, 

and all-age mortality is also three times larger for results based on Jerrett et al. (2009) effect 

estimates, indicating that the larger estimate does not simply result from a longer modeling 

period or different population subset (e.g. adult respiratory disease for Jerrett et al. (2009) effect 

estimates versus all-age non-accidental or all-cause mortality for Smith et al. (2009) and 

Zanobetti and Schwartz (2008) effect estimates). Recent studies using long-term O3-mortality 

relationships found by Jerrett et al. (2009) to quantify the burden of mortality due to 

anthropogenic O3 globally (Anenberg et al., 2010, 2011) and for the U.S. specifically (Fann et 

al., 2012) have also found that using Jerrett et al. (2009) long-term effect estimates yields O3-

related mortality burden estimates that are approximately two to four times larger than estimates 

based on short-term effect estimates. Since long-term mortality relationships include both acute 

and chronic exposure effects, the significantly larger mortality estimates calculated using longterm concentration-mortality relationships suggest that considering only short-term mortality 

may exclude a substantial portion of O3-related risk. However, since the short-term mortality 

relationships include a larger population (all ages versus adults ages 30 and older only) and all 

mortality causes, the short-term mortality relationships may capture some O3 effects that are not 

captured by Jerrett et al. (2009). It is likely that some portion of the estimated premature deaths 

attributable to short-term O3 exposure is captured by estimated premature deaths attributable to 

long-term O3 exposure, but the extent of the overlap between these estimates is unknown. 

8.2 EVALUATING THE REPRESENTATIVENESS OF THE URBAN STUDY 

AREAS IN A NATIONAL CONTEXT 

To further support interpretation of risk estimates generated in Section 7.2, this section 

presents three analyses that assess the representativeness of the 12 urban study areas in the 

national context. First, we assess the degree to which the 12 urban study areas represent the 

range of air quality levels and key O3 risk-related attributes that vary spatially across the nation. 

We have partially addressed this issue by selecting urban study areas in different geographical 

regions of the country (see Section 7.2). In this section, we evaluate how well the selected urban 

areas represent the overall U.S. for a set of spatially-distributed O3 risk related variables (e.g. 
8-22 

weather, demographics including socioeconomic status, baseline health incidence rates; Section 

8.2.1). Section 8.2.2 identifies where our 12 urban study areas fall along the distribution of O3-

attributable mortality risk across the U.S. This analysis allows us to assess the degree to which 

the 12 urban study areas capture locations within the U.S. likely to experience elevated levels of 

risk related to ambient O3. Finally, we give a national context to the estimated O3 responses to 

emission changes in the urban study areas by assessing how well these 12 areas and the 3 

additional exposure assessment study areas represent air quality trends and responses to 

emissions across the entire U.S. (Section 8.2.3). 

We do not attempt to assess the representativeness of the 15 urban study areas considered 

in the exposure assessment for O3 related risk because data limitations preclude us from being 

able to characterize individual-level exposure across the U.S. However, the urban study areas 

considered in both the exposure and risk assessments shared common selection criteria, 

including consideration of O3 concentrations, availability of adequate monitoring data, 

demographics, and exposure factors. Therefore, conclusions from this analysis of the 

representativeness of the 12 urban study areas for risk would also apply to those areas for 

exposure. 

8.2.1 Analysis Based on Consideration of National Distributions of Risk-Related 

Attributes 

This section evaluates how well the urban study areas reflect national-level variability in 

a series of O3 risk-related variables. For this analysis, we first generate distributions for riskrelated variables across the U.S. and for the specific urban study areas considered in Section 7.2 

from generally available data (e.g. from the 2000 Census, Centers for Disease Control (CDC), or 

other sources). We then plot the specific values of these variables for the selected urban study 

areas on these distributions, and evaluate how representative the selected study areas are of the 

national distributions for these individual variables. 

Estimates of risk (either relative or absolute, e.g., number of cases) within our risk 

assessment framework are based on four elements: population, baseline incidence rates, air 

quality, and the coefficient relating air quality and the health outcome (i.e. the O3 effect 

estimates). Each of these elements can contribute to heterogeneity in risk within and across urban 

study areas. In addition, there may be other identifiable factors that contribute to the variability 

of the four elements across urban study areas. In this assessment, we examine the 

representativeness of the selected urban study areas for the four main elements, as well as factors 

that have been identified as influential in determining the magnitude of the C-R function across 

urban study areas. 
8-23 

While personal exposure is not incorporated directly into O3 epidemiology studies, cityspecific O3 effect estimates are affected by differing levels of exposure which in turn are related 

to variability in exposure determinants. The correlation between monitored O3 and personal O3

exposure also varies between cities. The O3 ISA has comprehensively reviewed epidemiological 

and toxicological studies to identify variables which may affect the O3 effect estimates used in 

the city-specific risk analysis in Section 7.2 and the national-scale risk analysis in Section 8.1 

(U.S. EPA 2013). Determinants of the O3 effect estimates used in risk assessment can be grouped 

into four broad areas: 

 Demographics: education, income, age, unemployment rates, race, body mass index and 

physical conditioning, public transportation use, and time spent outdoors. 

 Baseline health conditions: asthma, chronic obstructive pulmonary disease, 

cardiovascular disease (atherosclerosis, congestive heart disease, atrial fibrillation, 

stroke), diabetes, inflammatory diseases, and smoking prevalence. 

 Climate and air quality: O3 levels, co-pollutant levels (annual mean PM2.5), temperatures 

(days above 90 degrees, mean summer temp, 98th percentile temp). 

 Exposure determinants: air conditioning prevalence. 

Although data limitations preclude our ability to conduct a national-scale exposure 

assessment as we have done for O3-attributable risk in Section 8.1, we assess the 

representativeness of the urban study areas across the national distribution of climate, air quality, 

and air conditioning prevalence, factors which influence individual exposure. As discussed in 

detail in Chapter 5, no available data base is sufficient to assess the national representativeness of 

time spent outdoors, another important personal exposure determinant, among persons residing 

in each of the urban study areas. However, previous analyses suggest that children’s time spent 

outdoors varies little across U.S. regions (section 8.10.2 of U.S. EPA, 2009). In addition, as 

discussed in Section 5.4.1, time spent outdoors and the percent of person-days having at least one 

minute outdoors (participation rate) does not appear to vary much over the past few decades 

based on analyses using the CHAD database, nor does there appear to be a temporal trend over 

the past decade based on analyses using the American Time Use Survey (ATUS). In considering 

that many of the activity pattern studies in CHAD were from national surveys conducted in 

metropolitan areas and that the evaluation results indicate little difference in time expenditure 

over broad geographic areas and survey collection years, it is likely that the distribution of time 

spent outdoors generated for the simulated persons in the 15 urban study areas (Chapter 5) 

reasonably reflects the most important elements of a national distribution of time spent outdoors. 

In addition, we were unable to assess the representativeness of the urban study areas in 

terms of fine-scale spatial variability in exposure, including near-roadway gradients. Cities with 

large populations living along highly trafficked roadways are expected to have higher O3
8-24 

exposure rates than cities with greater geographical separation between busy roadways and 

residential areas. Differences in near-roadway and other highly local exposure patterns contribute 

to heterogeneity among city-specific C-R functions, which are directly compared for this 

representativeness analysis. However, we are unable to make specific conclusions as to the 

differences in near-roadway and other highly local exposures among the urban study areas and 

between the urban study areas and the national distribution. 

Based on these identified potential risk determinants, we identify datasets that could be 

used to generate nationally representative distributions for each parameter. We are not able to 

identify readily available national datasets for all variables. In these cases, if we are able to 

identify a broad enough dataset covering a large enough portion of the U.S., we use that dataset 

to generate the parameter distribution. In addition, we are not able to find exact matches for all of 

the variables identified through our review of the literature. In cases where an exact match is not 

available, we identify proxy variables to serve as surrogates. For each parameter, we report the 

source of the dataset, its degree of coverage, and whether it is a direct measure of the parameter 

or a proxy measure (Table 8-6). Summary statistics for the most relevant variables are provided 

in Table 8-7. 
8-25 

Table 8-6. Data Sources for O3 Risk-related Attributes. 

Potential Riskrelated Attribute Attribute Metric Year Source 

Demographics Age Percent age 85 years 

and older 

2005 County Characteristics, 2000-2007 Inter-university 

Consortium for Political and Social Research 

Age Percent age 65 years 

and older 

2005 County Characteristics, 2000-2007 Inter-university 

Consortium for Political and Social Research 

Age Percent age 14 years 

and younger 

2005 County Characteristics, 2000-2007 Inter-university 

Consortium for Political and Social Research 

Education Population with less 

than high school diploma 

2000 USDA/ERS, http://www.ers.usda.gov/Data/Education/ 

Unemployment Percent unemployed 2005 County Characteristics, 2000-2007 Inter-university 

Consortium for Political and Social Research 

Income Per capita personal 

income 

2005 County Characteristics, 2000-2007 Inter-university 

Consortium for Political and Social Research 

Race Percent nonwhite 2006 County Characteristics, 2000-2007 Inter-university 

Consortium for Political and Social Research 

Population Total population 2008 Cumulative Estimates of Resident Population Change f

United States, States, Counties, Puerto Rico, and PuerRico Municipios: April 1, 2000 to July 1, 2008, Source: Population Division, U.S. Census Bureau 

Population density Population/square mile 2008 Cumulative Estimates of Resident Population Change f

United States, States, Counties, Puerto Rico, and PuerRico Municipios: April 1, 2000 to July 1, 2008, Source: Population Division, U.S. Census Bureau (calculated “acrow flies”) 

Urbanicity ERS Classification 

Code 

2003 County Characteristics, 2000-2007 Inter-university 

Consortium for Political and Social Research 
8-26 

Potential Riskrelated Attribute Attribute Metric Year Source 

Climate and Air Quality O3 levels Monitored 4th high daily 

maximum 8-hr average 

2007 EPA Air Quality System (AQS) 

O3 levels Seasonal mean of the 

daily maximum 8-hr average 

Avg. 2006-

2008 

AQS 

O3 levels Seasonal mean of the 

daily maximum 1-hr 

Avg. 2006-

2008 

AQS 

O3 levels Seasonal mean Avg. 2006-

2008 

AQS 

PM2.5 levels Monitored annual mean 2007 AQS Temperature Mean July temp 1941-1970 County Characteristics, 2000-2007 Inter-university 

Consortium for Political and Social Research 

Relative Humidity Mean July RH 1941-1970 County Characteristics, 2000-2007 Inter-university 

Consortium for Political and Social Research 

Exposure DeterminantsVentilation Percent residences with 

no air conditioning 

2004 American Housing Survey 

Baseline Health Conditions Baseline mortality All Cause CDC Wonder 1999-2005 Baseline mortality Non Accidental CDC Wonder 1999-2006 Baseline mortality Cardiovascular CDC Wonder 1999-2007 Baseline mortality Respiratory CDC Wonder 1999-2008 Baseline morbidity Acute myocardial 

infarction prevalence 

2007 Behavioral Risk Factor Surveillance System (BRFSS) 

Baseline morbidity Diabetes prevalence 2007 BRFSS Baseline morbidity Stroke prevalence 2007 BRFSS 
8-27 

Potential Riskrelated Attribute Attribute Metric Year Source 

Baseline morbidity Congestive heart 

disease prevalence 

2007 BRFSS 

Obesity Body Mass Index 2007 BRFSS Level of exercise Vigorous activity 20 

minutes 

2007 BRFSS 

Level of exercise Moderate activity 30 

minutes or vigorous activity 20 minutes 

2007 BRFSS 

Respiratory risk factors 

Current asthma 2007 BRFSS 

Smoking Ever smoked 2007 BRFSS C-R Estimates Mortality risk Non Accidental 2009 Smith et al. (2009) Mortality risk All Cause 2008 Zanobetti and Schwartz (2008) Mortality risk Cardiovascular 2008 Zanobetti and Schwartz (2008) Mortality risk Respiratory 2008 Zanobetti and Schwartz (2008) 
8-28 

Table 8-7. Summary Statistics for Selected O3 Risk-related Attributes. 

Average Standard Deviation Maximum Mi

Risk-related Attribute 

Urban 

Study 

Areas 

U.S. 

Dataset 

Urban 

Study 

Areas 

U.S. 

Dataset 

Urban 

Study 

Areas 

U.S. 

Dataset 

Urban 

Study 

Areas 

Demographics Population per county 1,642,198 97,020 1,972,403 312,348 9,862,049 9,862,049 354,361 Population density (Pop/sq mile) 10,378 258 16,550 1,757 71,758 71,758 1,313 Median age (Years) 35.7 38.6 2.3 4.4 40.0 55.3 32.1 % Age 0 to 14 years 20.7 19.0 2.4 2.9 24.6 36.8 14.7 % Age 65+ years 11.3 14.9 2.5 4.1 15.2 34.7 5.8 % Age 85+ years 1.7 2.1 0.6 0.9 2.5 7.7 0.5 Unemployment rate (%) 5.7 5.4 1.2 1.8 8.6 20.9 4.1 % with less than high school diploma 20.9 22.6 7.9 8.8 37.7 65.3 8.7 Income per capita ($) 40305 27367 14238 6604 93377 93377 23513 % Non-white 36.4 13.0 15.3 16.2 86.7 95.3 31.7 % Commute by public transportation* 7.1 1.6 8.1 2.5 30.7 30.7 1.5 Health Conditions Prevalence of CHD (%) * 3.6 4.3 0.8 1.3 4.6 8.7 2.6 Prevalence of asthma (%) * 8.5 8.1 1.3 1.9 11.2 13.2 6.0 Prevalence of diabetes (%) * 8.1 8.5 1.2 2.1 10.6 16.5 5.4 Prevalence of AMI (%) * 3.6 4.1 0.6 1.3 4.8 10.2 2.8 Prevalence of obesity (%) * 24.7 26.0 4.0 4.1 32.7 35.7 18.7 Prevalence of stroke (%) * 2.6 2.7 0.7 1.0 3.7 6.5 1.5 Prevalence of ever smoked (%)* 18.3 19.6 3.1 4.0 23.1 34.4 14.2 Prevalence of exercise (20 minutes, %)* 29.5 28.0 2.7 4.8 33.8 44.1 23.7 Prevalence of exercise (30 minutes,%)* 50.2 49.7 2.3 5.4 55.3 67.1 47.4 Non-accidental mortality (deaths per 100,000 people) 756.2 950.6 204.1 249.6 1139.5 1958.4 361.6 
8-29 

Average Standard Deviation Maximum Mi

Risk-related Attribute 

Urban 

Study 

Areas 

U.S. 

Dataset 

Urban 

Study 

Areas 

U.S. 

Dataset 

Urban 

Study 

Areas 

U.S. 

Dataset 

Urban 

Study 

Areas 

All cause mortality (deaths per 100,000 people) 810.1 1022.3 217.4 258.6 1257.8 2064.2 402.5 Cardiovascular mortality (deaths per 100,000 people) 310.5 392.1 93.9 121.0 459.6 970.4 122.4 Respiratory mortality (deaths per 100,000 people) 66.2 97.3 17.0 32.3 90.1 351.0 34.8 Air Quality and Climate O3 4th high daily maximum 8-hr 

average (ppm) 0.087 0.077 0.009 0.010 0.105 0.126 0.072 

O3 seasonal mean (ppb) 33.9 34.5 5.4 6.6 51.0 64.8 25.8 O3 seasonal mean of daily 

maximum 8-hr average (ppb) 50.7 48.6 7.5 7.2 70.2 79.7 40.8 

O3 seasonal mean of daily 

maximum1-hr (ppb) 58.8 54.7 7.5 8.0 85.1 92.4 46.5 

PM2.5 annual mean (μg/m3) 14.1 11.7 2.6 3.1 16.9 22.5 8.4 PM2.5 98th %ile daily average 

(μg/m3) 35.8 30.7 8.1 9.3 59.0 81.1 21.2 

Average temperature (°F) 57.2 57.2 5.0 7.9 70.3 76.2 50.1 July temperature long term average (°F) 76.0 75.9 3.4 5.4 83.3 93.7 68.5 July Relative Humidity long term average (%) 61.5 56.2 10.2 14.6 70.0 80.0 28.0 Exposure Determinants 

% No air conditioning* 15.5 16.6 85.7 79.1 42.9 86.7 0.4 

C-R Estimates Non-accidental mortality O3 risk* 0.000388 0.000322 0.000217 0.000131 0.000917 0.000917 0.000148 All Cause mortality O3 risk* 0.000627 0.000527 0.000314 0.000205 0.001092 0.001092 0.000163 Respiratory mortality O3 risk* 0.000877 0.000800 0.000282 0.000186 0.001424 0.001424 0.000307 Cardiovascular mortality O3 risk* 0.000898 0.000825 0.000173 0.000124 0.001064 0.001064 0.000418 

*Attribute for which only city-specific data were available.
8-30 

Figure 8-12 through Figure 8-18 show national-level cumulative distribution functions 

(CDF) for the four critical risk function elements (population, air quality, baseline incidence, and 

the O3 effect estimate), as well as where the urban study areas fall on the distribution. While the 

urban-scale analysis in Chapter 7 includes the full core-based statistical area for the selected 

cities, we consider here only the counties included in each city as defined by the epidemiological 

studies, since we only have information on O3 effect estimates for these counties. This approach 

is consistent with the national-scale assessment of O3-attributable risk in Section 8.1, from which 

we draw county-level O3-attributable risk estimates for the representativeness analysis in Section 

8.2.3. These figures focus on critical variables representing each type of risk determinant, e.g. we 

focus on all-cause and non-accidental mortality rates, but we also have conducted analyses for 

cardiovascular and respiratory mortality separately. The vertical black lines in each graph show 

the values of the variables for the individual urban study areas. The city-specific values that 

comprise the national CDF for mortality risks found by Zanobetti and Schwartz (2008) are also 

displayed on the graphs of those attributes, as the number of cities included in that study is 

smaller (48 cities). The complete analysis is provided in Appendix 4A. 

These figures show that the selected urban study areas represent the upper percentiles of 

the distributions of population and do not represent the locations with lower populations (urban 

study areas are all above the 90th percentile of U.S. county populations). This is consistent with 

the objectives of our case study selection process, e.g. we are characterizing risk in areas that are 

likely to be experiencing excess risk due to O3 levels above alternative standards. The urban 

study areas span the full range of seasonal means of the daily maximum 8-hr average O3

concentrations in monitored U.S. counties and the full distribution of O3 risk coefficients across 

the cities included by Smith et al. (2009) and Zanobetti and Schwartz (2008). The urban study 

area analysis includes the two cities with the highest risk coefficients found by Smith et al. 

(2009) – New York City and Philadelphia – as well as the two highest found by Zanobetti and 

Schwartz (2008) – New York City and Detroit. In Table 8-7, respiratory and cardiovascular 

mortality have higher C-R relationships than non-accidental and all-cause mortality because they 

are based on a smaller baseline population and are the diseases most affected by O3 exposure. 

The urban study areas do not capture the upper end of the distribution of baseline mortality, 

including all-cause (Figure 8-15) and non-accidental mortality (Figure 8-16), as well as 

cardiovascular and respiratory mortality (see Appendix 8B). The interpretation of this is that the 

case study risk estimates may not capture the additional risk that may exist in locations that have 

the highest baseline mortality rates. 
8-31 

Figure 8-12. Comparison of County-level Populations of Urban Study Area Counties to the 

Frequency Distribution of Population in 3,143 U.S. Counties. 

Figure 8-13. Comparison of County-level Seasonal Means of the Daily Maximum 8-hr 

Average O3 Concentrations in Urban Study Area Counties to the Frequency Distribution of 

Seasonal Mean of the Daily Maximum 8-hr O3 Concentrations in 671 U.S. Counties with O3 

Monitors. 
8-32 

Figure 8-14. Comparison of 2007 County-level 4th highest Daily Maximum 8-hr Average 

O3 Concentrations in Urban Study Area Counties to the Frequency Distribution of 2007 4th

highest Daily Maximum 8-hr Average O3 Concentrations in 725 U.S. Counties with O3 

Monitors. 

Figure 8-15. Comparison of County-level all-cause Mortality in Urban Study Area 

Counties to the Frequency Distribution of all-cause Mortality in 3,137 U.S. Counties. 
8-33 

Figure 8-16. Comparison of County-level non-accidental Mortality in Urban Study Area 

Counties to the Frequency Distribution of non-accidental Mortality in 3,135 U.S. Counties 

Figure 8-17. Comparison of City-level all-cause Mortality Risk Coefficients from Zanobetti 

and Schwartz (2008) in Urban Study Areas to the Frequency Distribution of all-cause 

Mortality Risk Coefficients from Zanobetti and Schwartz (2008) in 48 U.S. Cities. 
8-34 

Figure 8-18. Comparison of City-level National-prior Bayes-shrunken non-accidental 

Mortality Risk Coefficients from Smith et al. (2009) in Urban Study Areas to the 

Frequency Distribution of National-prior Bayes-shrunken non-accidental Mortality Risk 

Coefficients from Smith et al. (2009) in 98 U.S. Cities 

Figure 8-19 through Figure 8-24 show national CDFs and the urban study area values for 

several selected potential risk attributes. These potential risk attributes do not directly enter the 

risk equations, but have been identified in the literature as potentially affecting the magnitude of 

the O3 C-R functions reported in the epidemiological literature. Comparison graphs for other risk 

attributes are provided in Appendix 4A. The selected urban study areas do not capture the higher 

end percentiles of several risk characteristics, including populations 65 years and older, baseline 

cardiovascular disease prevalence, baseline respiratory disease prevalence, and smoking 

prevalence. Summarizing the analyses of the other risk attributes, we conclude that the urban 

study areas provide adequate coverage across population, population density, O3 levels (seasonal 

mean, seasonal means of the daily maximum 8-hr, and seasonal means of the daily maximum 1-

hr), PM2.5 co-pollutant levels, temperature and relative humidity, unemployment rates, percent 

non-white population, asthma prevalence obesity prevalence, income, and less than high school 

education. We also conclude that while the urban study areas cover a wide portion of the 

distributions, they do not provide coverage for the upper end of the distributions of percent of 

population 65 and older (below 60th percentile), percent of population 85 years and older (below 

75th percentile), prevalence of angina/coronary heart disease (below 70th percentile), prevalence 

of diabetes (below 85th percentile), stroke prevalence (below 90th percentile), prevalence of heart 

attack (below 80th percentile), prevalence of smoking (below 85th percentile), all-cause mortality 
8-35 

rates (below 85th percentile), non-accidental mortality rates (below 80th percentile), 

cardiovascular mortality rates (below 75th percentile) and respiratory mortality rates (below 50th

percentile), and percent of residences without air conditioning (below 90th percentile). In 

addition, the urban study areas do not capture the highest or lowest ends of the distribution of 

exercise prevalence and do not capture the low end of the distribution of public transportation 

use (above the 65th percentile). 

Figure 8-19. Comparison of County-level Percent of Population 0 to 14 years old in Urban 

Study Area Counties to the Frequency Distribution of Percent of Population 0 to 14 years 

old in 3,141 U.S. Counties. 
8-36 

Figure 8-20. Comparison of County-level Percent of Population age 65 years old and older 

in Urban Study Area Counties to the Frequency Distribution of Percent of Population age 

65 and older in 3,141 U.S. Counties. 

Figure 8-21. Comparison of County-level Income per capita in Urban Study Areas to the 

Frequency Distribution of Income per capita in 3,141 U.S. Counties. 
8-37 

Figure 8-22. Comparison of County-level July Temperature in Urban Study Area Counties 

to the Frequency Distribution of July Temperature in all U.S. Counties. 

Figure 8-23. Comparison of City-level Asthma Prevalence in Urban Study Areas to the 

Frequency Distribution of Asthma Prevalence in 184 U.S. Cities. 
8-38 

Figure 8-24. Comparison of City-level Air Conditioning Prevalence in Urban Study Areas 

to the Frequency Distribution of Air Conditioning Prevalence in 76 U.S. Cities. 

Based on the above analyses, we can draw several inferences regarding the 

representativeness of the urban study areas. First, the selected urban study areas are among the 

most populated in the U.S. Second, they represent urban areas with relatively high levels of O3

(4th highest daily maximum 8-hr average, seasonal mean of the daily maximum 8-hr average, 

seasonal mean of the daily maximum1-hr, and seasonal mean). Third, they capture well the range 

of city-specific effect estimates found by Smith et al. (2009) and Zanobetti and Schwartz (2008) 

studies. These three factors would suggest that the urban study areas should capture well overall 

risk for the nation, with a potential for better characterization of the high end of the risk 

distribution. 

However, there are several other factors that suggest that the urban study areas may not 

be representing areas that may have a high risk per ppb of O3. Several of the factors with 

underrepresented tails, including age and baseline mortality are spatially correlated (R=0.81), so 

that certain counties which have high proportions of older adults also have high baseline 

mortality and high prevalence of underlying chronic health conditions. Because of this, omission 

of certain urban areas with higher percentages of older populations, for example, cities in 

Florida, may lead to underrepresentation of high risk populations. However, with the exception 

of areas in Florida, most locations with high percentages of older populations have low overall 

populations, less than 50,000 people in a county. And even in Florida, the counties with the 

highest O3 levels do not have a high percent of older populations. This suggests that while the 
8-39 

risk per exposed person per ppb of O3 may be higher in these locations, the overall risk to the 

population is likely to be within the range of risks represented by the urban study locations. 

Due to data limitations, we were only able to assess the representativeness of the urban study 

areas in terms of one exposure-related attribute, air conditioning prevalence. Assessing the 

representativeness of the urban study areas in terms of air conditioning prevalence, we found that 

the urban study areas do not capture the highest end of percent of residences without air 

conditioning. If the cities with the lowest air conditioning prevalence also have high O3 levels, 

we could be missing a high risk portion of the population that is exposed to O3 indoors as air 

infiltrates indoors from outdoors. However, 4th highest daily maximum 8-hr averageO3 levels in 

the cities in the top 10th percentile of percentage of residences without air conditioning (mainly 

in northern California and Washington) are approximately average (0.08 ppm) or lower than 

average. Since these concentrations are not the highest found across the U.S., we are likely not 

excluding a high risk population that has both low air conditioning prevalence and high O3

concentrations, and the overall risk to the population is likely to be within the range of risks 

represented by the urban study areas. 

8.2.2 Analysis Based on Consideration of National Distribution of Ozone-Related 

Mortality Risk 

In this section we discuss the second representativeness analysis which identifies where 

the 12 urban study areas examined in Chapter 7 fall along the distribution of estimated nationalscale mortality risk. This assessment reveals whether the baseline O3 mortality risks in the 12 

urban study areas represent more typical or higher end risk relative to the national risk 

distribution presented in Section 8.1. For consistency, we compare the national O3 mortality risk 

distribution to the O3 mortality risk results for the urban study areas that were generated from the 

national-scale assessment in Section 8.1, rather than the results from the urban study area 

analysis in Chapter 7 which uses different methods. To be consistent with the national-scale 

assessment, we define the urban study areas here as they were defined in the epidemiology 

studies, rather than including full core-based statistical areas as in Chapter 7. The results of this 

representativeness analysis are presented graphically in Figure 8-25 through Figure 8-27, which 

display the cumulative distribution of total mortality attributable to ambient O3 at the county 

level developed as part of the national-scale analysis. Values for the 23 counties included in the 

urban study areas as defined in the epidemiology studies are then superimposed on top of the 

cumulative distribution to assess the representativeness of the urban study areas. 

For the results based on Smith et al. (2009) effect estimates, New York City and 

Philadelphia have the highest percentage of May-September non-accidental mortality attributable 

to ambient O3 of the 12 urban study areas and are located at the highest end of the distribution of 
8-40 

U.S. O3-related mortality risk (Figure 8-25). Of the 12 urban study areas, these two cities had the 

highest effect estimates found by Smith et al. (2009; See Appendix 4A). Boston and Los Angeles 

had the lowest O3-related mortality risk of the 12 urban study areas and are located at the lowest 

end of the U.S. distribution. Overall, O3 mortality risk in the 12 urban study areas are 

representative of the full distribution of U.S. O3-related mortality risk, with the mean percentage 

of May-September non-accidental mortality for all ages of 1.5% (95% confidence interval, 1.1-

1.8%). 

For the results based on Zanobetti and Schwartz (2008) effect estimates, Detroit and New 

York City are at the very highest end of the U.S. distribution of county-level risk of June-August 

all-cause mortality due to ambient O3 (Figure 8-26). These two cities had the highest effect 

estimates of the 48 cities included in the study (see Appendix 4A). The high effect estimates in 

Detroit and New York City could be due to high rates of public transportation use (for New York 

City), low air conditioning prevalence, high smoking prevalence (in Detroit), high incidence of 

mortality and other adverse health outcomes (e.g. diabetes, stroke, acute myocardial infarction, 

etc.), and high unemployment rates. Houston and Los Angeles had the lowest risk and were 

located at the very lowest end of the U.S. distribution of county-level risk of mortality due to 

ambient O3. These two cities had the lowest effect estimates found by Zanobetti and Schwartz 

(2008), possibly because they cover a large spatial extent and have high rates of time spent 

driving, which could lead to exposure misclassification in the underlying epidemiologic study. 

Houston also has a very high rate of air conditioning use (nearly 100% of residences) and Los 

Angeles has been shown to have high rates of adaptive behavior on high ambient O3 days (i.e. 

more time spent indoors as a result of high ambient O3 concentrations; Neidell 2009, 2010), both 

of which would lead to lower personal O3 exposure relative to other cities. Overall, O3 mortality 

risk in the 12 urban study areas are representative of the full distribution of U.S. O3-related 

mortality risk, with the mean percentage of June-August all-cause mortality for all ages of 2.5% 

(95% confidence interval, 1.7-3.0%). 

For the results based on Jerrett et al. (2009) effect estimates, the 12 urban study areas are 

centered more in the middle of the distribution of U.S. county-level risk of adult (ages 30 and 

older) respiratory mortality due to ambient O3 exposure. These results are based on the 

application of a single national average effect estimate to all grid cells across the U.S., rather 

than city-specific effect estimates as were applied for the results based on Smith et al. (2009) and 

Zanobetti and Schwartz (2008) effect estimates. Therefore, the location of the urban study areas 

on the distribution of county-level risk is driven mainly by O3 concentration and not by the effect 

estimate. While Denver, Atlanta, Sacramento, and Los Angeles are at the highest end of the U.S. 

distribution, Figure 8-27 shows that some counties have a higher percentage of mortality 

attributable to O3 than these four cities. Overall, O3 mortality risk in the 12 urban study areas are 
8-41 

representative of the full distribution of U.S. O3-related mortality risk, with the mean percentage 

of April-September respiratory mortality for adults ages 30 and older of 18.7% (95% confidence 

interval, 15.2-21.5%). However, we are not capturing the very highest end of O3-related risk 

based on Jerrett et al. (2009) effect estimates in the 12 urban study areas. 

Figure 8-25. Cumulative Distribution of County-level Percentage of May-September nonaccidental Mortality for all ages Attributable to 2006-2008 Average O3 for the U.S. and the 

Locations of the Selected Urban Study Areas along the Distribution, using Smith et al. 

(2009) Effect Estimates. 
8-42 

Figure 8-26. Cumulative Distribution of County-level Percentage of June-August all-cause 

Mortality for all ages Attributable to 2006-2008 Average O3 for the U.S. and the Locations 

of the Selected Urban Study Areas along the Distribution, using Zanobetti and Schwartz 

(2008) Effect Estimates. 

Figure 8-27. Cumulative Distribution of County-level Percentage of April-September 

Adult (age 30+) Respiratory Mortality Attributable to 2006-2008 Average O3 for the U.S. 

and the Locations of the Selected Urban Study Areas along the Distribution, using Jerrett 

et al. (2009) Effect Estimates and City Definitions from Zanobetti and Schwartz (2008). 
8-43 

8.2.3 Analysis Based on Consideration of National Responsiveness of Ozone 

Concentrations to Emissions Changes 

Estimates of O3 response to precursor emissions reductions (NOx and VOC) are 

important inputs to estimation of risk for scenarios of just meeting existing and alternative O3

standards. To evaluate the national representativeness of O3 responses to decreases in precursor 

emissions in the 15 urban study areas, we examine two different types of air quality data. In 

section 8.2.3.1 we examine ambient O3 trends that have been measured at monitor locations 

across the country over a recent period of decreasing NOx emissions. This analysis provides realworld observations but does not isolate the effects of emissions changes alone and can only 

characterize past phenomena. In section 8.2.3.2, we look at air quality model predictions of 

temporal and spatial patterns of O3 changes in response to further NOx reductions from 2007 

levels. This analysis is subject to typical model limitations but has the advantage of isolating the 

effects of precursor emissions changes and has the ability to simulate how O3 would change in 

response to NOx (and VOC) emissions reductions (relative to recent 2007 levels) similar to those 

used in the HDDM adjustment scenarios for just meeting existing and alternative standards. 

These two complimentary analyses give qualitatively similar results, building confidence that the 

overarching conclusions are robust across the U.S. as a whole. 

8.2.3.1 Ambient patterns in trends of measured ozone concentrations 

This section describes how annual distributions of O3	measurements collected by EPA's 

national monitoring network have changed between 1998 and 2011. These years were chosen 

because large reductions in anthropogenic NOx emissions have occurred over this time period 

especially in the Eastern half of the United States. From 2000 to 2011 nationwide NOx emissions 

were cut almost in half (from 22.6 to 12.9 million tons per year).3 However, it should be noted 

that these reductions did not occur uniformly across the country. Improvements in vehicle 

emissions standards helped reduce NOx emissions in many locations throughout the country. In 

contrast, EPA rules like the NOx SIP call were focused on controlling emissions from power 

plants in the Eastern US and consequently there have been relatively larger reductions in NOx

emissions in the East. In addition, some urban areas which have traditionally had high O3 levels, 

like Los Angeles and Houston, have substantially cut local NOx and VOC emissions to improve 

their air quality. Also, there may be some localized areas in which NOx emissions have increased 

due to population growth, new sources such as oil and gas development, or increased wildfire 

activity. Appendix 8C provides plots of emissions trends by region of the U.S. These plots show 

that each of nine regions of the U.S. have experienced decreasing NOx emissions ranging from 

 

3

 Data were accessed from EPA’s emission trend website on August 15, 2013: 

http://www.epa.gov/ttn/chief/trends/trends06/national_tier1_caps.xlsx 
8-44 

approximately a 20% decrease to a 45% decrease from 2002 to 2011 depending on the region. 

Conversely, VOC emissions have increased in some regions since 2002 (the South, the 

Southwest, and the West-North-Central) and decreased in others. Due to non-linear O3 formation 

chemistry and the potential for changes in local chemical regimes resulting from these emissions 

reductions, past trends may not reflect the ambient changes which will occur from future 

emissions reductions. Nonetheless, these ambient data provide information on actual O3 changes 

in response to emissions reductions and can give insight into the types of changes in O3 that have 

occurred both within and outside the urban study areas. 

First, we look at national maps which show changes in 50th percentile and 95th percentile 

summer season (April-October)4 daily maximum 8-hr O3 values (Figure 8-28, Figure 8-29). 

These maps reflect the absolute (ppb) difference between O3 percentiles from two three-year 

periods (2001-2003 and 2008-2010)5

. Figure 8-28 shows that increases in median O3

concentrations occurred in many large urban areas including both study area locations in Chapter 

76

 and non-study area locations7. Only a few monitors with increasing median O3 appear outside 

of cities, most notably in southwestern Colorado and central Kansas. The increases in urban 

areas are likely explained by O3 disbenefits in response to NOx reductions which were described 

in Chapter 4, Appendix 4C and in the following section of this chapter. Widespread decreases of 

median O3 in suburban and rural locations suggest the efficacy of large NOx emissions 

reductions on reducing O3 over large regions of the country. Finally, the less frequently observed 

cases of median O3 increases in rural areas are likely caused by different phenomena. Cooper et 

al. (2012) suggested that increasing rural O3 in the Western US may be due to increasing oil and 

gas development, wildfires and O3 transport from Asia. Conversely, Figure 8-29 shows that 95th

percentile O3 values for these two sets of years decrease in almost all urban as well as rural areas 

of the country. Only a few sites in Colorado, Nevada, and California show any increases in 95th

percentile O3 between 2001-2003 and 2008-2010. The consistent decreases across most of the 

United States indicate that the large NOx reductions from power plants and mobile sources have 

 

4

 The April-October time period corresponds to the required monitoring season for most of the 12 urban areas. 

Therefore, in selecting a consistent time period that could be analyzed for the urban case study areas, we chose to 

use the April-October time period in Chapter 4 for composite monitor distributions to summarize O3

concentrations relevant to the epidemiological-based risk assessment. 

5

 These two three-year periods were chosen to represent years before and after most NOx emission reductions were 

in place. In addition the 2001-2003 period was used to designate areas for the 1997 8-hr O3 standard and the 2008-

2010 period was used to designate areas for the 2008 8-hr O3 standard. Data from these two time periods have 

undergone extensive quality checks. 6

 Los Angeles, Denver, Houston, Atlanta, Chicago, Detroit, Cleveland, New York, Philadelphia, and Washington 

D.C. 7

 San Francisco, Reno, Phoenix, New Orleans, Birmingham, Miami, and Cincinnati. 
8-45 

been quite successful in reducing O3 on the highest O3 days. These results suggest that many of 

the urban study areas may show O3 responses that are typical of other large urban areas in the 

U.S. However, decreasing O3 in large non-urban portions of the country may not be fully 

captured in the urban study areas. 

To examine these trends further, we evaluate the 1998-2011 data from the 15 case-study 

areas. Only monitors within the 15 study areas8 were analyzed, and within each study area, 

monitors were put into three groups based on the degree of urbanization. The degrees of 

urbanization were determined by the population density of the census tract containing the 

monitor (plotted in Figure 8-30). Population data were obtained from the U.S. Census Bureau9, 

and the classes were determined by breaks in the population density calculated from those data: 

“high population density" (> 1000 people/km2

), “medium population density" (between 400 and 

1000 people/km2

), and “low population density" (<	400 people/km2). Data were additionally split 

out into three different time periods (all months, warm months: May through September, and 

cool months: October through April). These warm and cool season categorizations were chosen 

to isolate effects that are observed at different times of year. The April-October time period 

which was examined in Figure 8-28 and Figure 8-29 include all warm season and two cold 

season months and thus show behavior that has influences from both. Summaries were thus 

calculated for groups of monitors specific to (1) Study Area, (2) Month subset, and (3) Urban 

class. 

 

8

 These 15 areas are the 12 urban case study areas in the epidemiological-based risk assessment and the 3 additional 

exposure urban case study areas. 9

 Obtained from: http://www2.census.gov/geo/tiger/TIGER2010DP1/Tract_2010Census_DP1.zip 
8-46 

Figure 8-28. Change in 50th Percentile Summer Season (April-October) Daily Maximum 8-

hr Average O3 Concentrations between 2001-2003 and 2008-2010. 

Figure 8-29. Change in 95th Percentile Summer Season (April-October) Daily Maximum 8-

hr Average O3 Concentrations between 2001-2003 and 2008-2010. 
8-47 

Figure 8-30. Population Density within Census Tract where each O3 Monitor is Located. 

Figure 8-31, Figure 8-32, and Figure 8-33 display the data described above in ribbon 

plots for high, medium, and low population density monitor locations in each case study area. 

The lines bordering the dark and light red ribbons in this plot are (from top to bottom) the 95th, 

75th, 25th, and 5th percentiles of the annual data indicated by each panel, and the median (i.e. 50th

percentile) is shown by the line in the middle of the central lighter ribbon. The colors of the lines 

separating the ribbons depict significant trends (dark blue for decreasing and light blue for 

increasing) or no significant trend (white). Statistical significance for multi-year O3 trends was 

determined using the Spearman rank order correlation coefficient (p-value < 0.05). Plots showing 

a characterization of the entire O3 distribution (not just discrete cut points of 5th, 25th, 50th, 75th, 

and 95th percentiles) are provided in Appendix 8C. 

These plots show consistent trends over the past 13 years for O3, with high O3 values 

decreasing fairly uniformly across different regions and areas of different degrees of 

urbanization. Conversely, mean and median trends appear quite different in high, medium, and 

low population density areas. Mid-range O3 concentrations at low population density locations 

within the case study areas (so still relatively close to a major city) have generally decreased over 

a period of substantial NOx emissions reductions.10 This decrease is most pronounced in the 

 

10 Denver is unique among the case study areas with consistently increasing mid-range O3 trends across seasons and 

urban classifications. Denver may be subject to increasing emissions from large wildfires and oil and gas 
8-48 

summer months and in the Eastern half of the U.S. (low population density monitors in 3 out of 

the 5 Western11 case-study areas and in only 4 out of the 10 Eastern12 case study areas do not 

have significant decreases in summertime median O3 concentrations). Mid-range O3

concentrations in many, but not all, high population density areas have significantly increased in 

winter months. Wintertime increases were significant in 11 of the 15 areas (only Atlanta, Boston, 

Houston and Sacramento did not increase significantly). Thirteen out of 15 summertime high 

population density area trends in median O3 were not significant,13 but combining winter and 

summer measurements to determine annual trends showed that Denver, Los Angeles, New York 

and Philadelphia high population density sites had significantly increasing annual median O3

while Boston, Chicago, Dallas and St. Louis had significantly increasing 25th percentile O3 but 

no significant median trend. These results reflect increasing mid-range O3 concentrations mainly 

confined to urban centers during periods of NOx reductions. One important point to note is that 

the design value monitor (the monitor with the highest average (over three years) of 4th highest 

daily maximum value) in most of the case-study locations is located outside of the high 

population density area (as defined here). Downward trends in medium and low population 

density areas are therefore generally representative of the behavior at the highest O3 monitor in 

an area, whereas trends in urban centers may be important from an exposure perspective. 

In summary, any increasing O3 trends occur more in highly populated areas, during cool months, 

and at the lower end of the O3 distribution. Conversely, any decreasing O3 trends occur more 

during warm months, in lower population areas, and at the upper end of the O3 distribution. One 

result of these two phenomena is a narrowing of the range of O3 concentrations over this period 

of decreasing NOx emissions. For instance, there are many cases where the top and bottom of a 

single distribution exhibit different trends. For example, the low population density monitors of 

Dallas, Los Angeles, Philadelphia and Saint Louis and the high population density monitors for 

Baltimore, Dallas, and Philadelphia for all months show a significant increase in the 5th

percentile and a simultaneous significant decrease in the 95th percentile. More common is a 

significant change in one end of the distribution, but no significant change in the other (e.g., the 

summer months at high population density monitors in all case study areas except Baltimore, 

Chicago, and Detroit). It is important to note that there are also cases where both ends of the 

distribution change in the same manner and there is therefore no narrowing of the range of O3

concentrations in these areas. 

 

development which are not typical of other urban case study areas. In addition, Denver is particularly susceptible 

to influences from stratospheric intrusions and international transport due to its high altitude. 11 Western case study areas for this purpose include: Dallas, Denver, Houston, Los Angeles, and Sacramento. 12 Eastern case study areas for this purpose include: Atlanta, Baltimore, Boston, Chicago, Cleveland, Detroit, New 

York, Philadelphia, St. Louis, and Washington D.C. 13 Only Houston and Dallas had statistically significant trends in median summertime urban O3. 
8-49 

Figure 8-31. Distributions of O3 Concentrations for High Population Density Monitors by 

Different Subsets of Months over a 13-year Period. From top to bottom in each ribbon plot, 

the blue and white lines indicate the spatial mean of the 95th, 75th, 50th, 25th, and 5th

percentiles for each monitor for every year from 1998-2011. 

Figure 8-32. Distributions of O3 Concentrations for Medium Population Density Monitors 

by Different Subsets of Months over a 13-year Period. From top to bottom in each ribbon 

plot, the blue and white lines indicate the spatial mean of the 95th, 75th, 50th, 25th, and 5th

percentiles for each monitor for every year from 1998-2011. 
8-50 

Figure 8-33. Distributions of O3 Concentrations for Low Population Density Monitors by 

Different Subsets of Months over a 13-year Period. From top to bottom in each ribbon plot, 

the blue and white lines indicate the spatial mean of the 95th, 75th, 50th, 25th, and 5th

percentiles for each monitor for every year from 1998-2011. 

Maps of ambient trends in both New York City and Chicago most clearly show these 

trends and further illustrate this behavior. Figure 8-34 and Figure 8-35 show trends in daily 

maximum 8-hr O3 values these two cities for May-September. Plots for other case-study areas 

are provided in Appendix 8C. For both cities, the 4th highest daily maximum 8-hr average O3

value either has a downward trend or no trend at all monitors. In New York (Figure 8-34), mean 

and median O3 values significantly decrease at downwind locations in New York and 

Connecticut. Conversely, median O3 values significantly increase from 1998 to 2011 at two core 

urban sites (one at City College of NY in upper Manhattan and one near Queen’s college) and at 

a nearby site on Long Island. Similarly, in Chicago (Figure 8-35), mean and median trends in O3

are downward or insignificant in Indiana and in suburban Illinois locations and show increases 

near the highly populated urban core. 
8-51 

Figure 8-34. Map of O3 Trends at Specific Monitors in the New York Area. All upward and downward fa

represent statistically significant trends from 1998-2011 (p < 0.05), circles represent locations with no signused in Smith et al (2009) and the Zanobetti and Schwartz (2008) epidemiology studies are represented by 

monitors with at least seven years of data are displayed. The pink star indicates the site with the higher de

The MSA border as defined by the U.S. census bureau is delineated by the light blue line. Left panel shows 

highest daily maximum 8-hr average O3 values, center panel shows trends in annual means of the daily ma

O3 values, and right panel shows trends in annual medians of the daily maximum 8-hr average O3 values. 
8-52 

Figure 8-35. Map of O3 Trends at Specific Monitors in the Chicago Area. All upward and downward facinrepresent statistically significant trends from 1998-2011 (p < 0.05), circles represent locations with no sign

used in Smith et al (2009) and the Zanobetti and Schwartz (2008) epidemiology studies are represented by 

monitors with at least seven years of data are displayed. The pink star indicates the site with the higher deThe MSA border as defined by the U.S. census bureau is delineated by the light blue line. Left panel shows highest daily maximum 8-hr average O3 values, center panel shows trends in annual means of the daily ma

O3 values, and right panel shows trends in annual medians of the daily maximum 8-hr average O3 values.
8-53 

To demonstrate how changes in emissions of NOx and anthropogenic VOCs might be 

driving these trends, Table 8-8 shows trends of O3 in high and low population areas and annual 

National Emissions Inventories (NEI) for 2002, 2005, 2008 and 201114 aggregated to the level of 

the NOAA Climate Regions.15 There is moderate correspondence between the decreases in NOx

emissions across the regions with the observed decreases in warm season O3 concentrations in 

low population areas. VOCs show little correspondence to any of the O3 trends, which is likely 

due to complications from (1) the mix of chemicals with a large range of reactivities; (2) 

complex non-linear chemistry; and (3) the potential impact of the much larger magnitude of 

biogenic vs. anthropogenic emissions on a regional scale. Details of these calculations can be 

found in Appendix 8C. 

Table 8-8. Broad Regional Annual Trends of Concurrent O3 Concentrations and 

Emissions of NOx and VOCs over years 2000-2011. 

Trend Central 

East 

North 

Central 

North 

East South 

South 

East 

South 

West West 

High Population 

Density, May-Sept 

O3

None None None Down None None None 

High Population 

Density, Oct-Apr O3 Up Up Up Low %’s 

up None Up Up 

Low Population 

Density, May-Sept 

O3

Down Down Down Down Down Low %’s 

up 

Top %’s 

down 

Low Population 

Density, Oct-Apr O3

None None Top %’s 

up None None Up None 

NOx Emission Down Down Down Down Down Down Down 

VOC Emission None None Down Up Down Up Down 

8.2.3.2 Modeled ozone response to emissions reductions across the United States 

This section presents an analysis of the CMAQ modeling of O3 responses to “across-theboard” U.S. anthropogenic precursor emissions reductions described in Appendix 4B. In this 

analysis, we compare the modeled responses of O3 concentrations in the case study areas to the 

modeled O3 responses in the rest of the U.S. For this purpose, we used five CMAQ model 

simulations: (1) a base simulation which included 2007 emissions of all O3 precursors, (2) a 50% 

NOx cut simulation in which U.S. anthropogenic NOx emissions were reduced by 50% from 

 

14 http://www.epa.gov/ttnchie1/trends/ 

15 http://www.ncdc.noaa.gov/monitoring-references/maps/us-climate-regions.php
8-54 

2007 levels, (3) a 90% NOx cut simulation in which U.S. anthropogenic NOx emission were 

reduced by 90% from 2007 levels, (4) a 50% NOx/VOC cut simulation in which both U.S. 

anthropogenic NOx and VOC emission were reduced by 50% from 2007 levels, and (5) a 90% 

NOx/VOC cut simulation. These simulations are analyzed to characterize responses in O3 to 

“across the board” emissions cuts at four distinct levels and do not represent the exact adjustment 

cases that were used to estimate O3 concentrations consistent with individual case study areas 

just meeting various potential levels of the NAAQS standard. However, these four cases 

generally span the range of emissions perturbations that were applied in the HDDM adjustment 

methodology described in Chapter 4 and in Appendix 4D. 

In this analysis we focus on seasonal mean O3 and population as proxies for 

epidemiology based risk estimates in Chapter 7. Since the epidemiology studies used in Chapter 

7 show relatively linear response of health outcomes to O3 concentrations throughout the entire 

range of measured O3 values, examining seasonal mean values should provide some 

understanding of locations where O3 health effects are expected to increase and decrease as a 

result of precursor emission reductions. By combining population information with these spatial 

distributions of seasonal O3 responses, we can better understand expected O3 behavior in 

locations where people live. This is not a detailed risk assessment but can provide information on 

the representativeness of the case-study areas to the nation as a whole in terms of expected O3-

related health outcomes. 

To begin, we examine maps displaying ratios of mean O3 concentrations in the emissions 

cut simulations to mean O3 concentrations in the 2007 base simulation. Figure 8-36 and Figure 

8-37 show the ratio of seasonal (April-October) mean O3 in the two NOx emissions reduction 

simulations to that in the base simulation for the entire model domain. Figure 8-38 and Figure 

8-39 depict the ratio of January mean O3 for the two NOx cut simulations. Figures showing the 

ratios based on the May-September seasonal average and figures for the NOx/VOC emissions 

reductions scenarios are provided in Appendix 8C. The maps show widespread decreases (i.e., 

ratios less than 1) in seasonal mean O3 across the country. These decreases are especially 

pronounced in the Eastern U.S. and in California. Ozone increases (i.e., ratios greater than 1) are 

confined to urban core areas except in January. The spatial extent of these O3 increases are 

generally less for the 90% NOx cut simulation than for the 50% NOx cut simulation although the 

magnitude is greater over very limited areas in Chicago, Seattle, and San Francisco. The O3

increases are most widespread in the cooler months (January, April, and October). For the AprilOctober seasonal average O3 concentrations, VOC in addition to NOx cuts did not substantially 

change the ratios of O3 in the emissions reduction scenarios to O3 in the base scenario. In the 

Northeast and Midwest, increases in seasonal mean O3 concentrations were mainly confined to 

urban study areas of New York, Detroit, Chicago, and St. Louis. In the Southeastern U.S., the 
8-55 

urban areas which show up as having increased seasonal mean O3 in the 50% NOx cut 

simulations include Miami, Orlando, Tampa, and New Orleans (only Miami has O3 increase in 

the 90% NOx cut simulation). The only case-study area in the southeast, Atlanta, does not 

experience increases in seasonal mean O3 in the model simulation (this is consistent with the 

changes in risk estimated for Atlanta, which show no increases in total risk as alternative 

standards are simulated). In the central U.S., seasonal mean O3 in the case study areas of Denver, 

Houston, and Dallas and non-case-study areas of San Antonio, Duluth, and Minneapolis 

increased with 50% NOx reductions. Seasonal mean O3 increases were seen only in Houston, 

Minneapolis, and Duluth with 90% reductions in simulated NOx emissions. The Northwestern 

U.S. showed some of the most widespread increases in seasonal mean O3 in the 50% and 90% 

NOx cut simulations covering the Seattle and Portland metro areas as well the San Francisco Bay 

area and in a single model grid cell for Sacramento (50% NOx reduction case only). Sacramento 

is the only city in the Northwest that was included as a case study area. Finally, Los Angeles (a 

case study area), San Diego, Phoenix, and Bakersfield were the areas for which CMAQ predicted 

seasonal mean O3 increases with the 50% NOx cut simulation. These O3 increases disappeared 

(or were largely diminished in the case of LA) in the 90% NOx cut case. Based on these maps, it 

appears that in the Northeast and the Central U.S., the case-study area selection likely 

oversampled these O3 increases on a geographic basis since all locations outside of city centers 

experienced decreasing seasonal mean O3 with the NOx reduction model simulations. However 

in two regions, the Southeast and the Northwest, the urban study area did not experience 

increases in seasonal mean O3 concentrations while other urban areas in the region did. In these 

two regions, the urban study area selection likely under-sampled the locations which experienced 

increases in seasonal mean O3. 
8-56 

Figure 8-36. Ratio of April-October Seasonal Average O3 Concentrations in the Bruteforce 50% NOx Emissions Reduction CMAQ Simulations to April-October Seasonal 

Average O3 Concentrations in the 2007 Base CMAQ Simulation. 

Figure 8-37. Ratio of April-October Seasonal Average O3 Concentrations in the Bruteforce 90% NOx Emissions Reduction CMAQ Simulations to April-October Seasonal 

Average O3 Concentrations in the 2007 Base CMAQ Simulation. 
8-57 

Figure 8-38. Ratio of January Monthly Average O3 Concentrations in Brute-force 50% 

NOx Emissions Reduction CMAQ Simulations to January Monthly Average O3

Concentrations in the 2007 Base CMAQ Simulation. 

Figure 8-39. Ratio of January Monthly Average O3 Concentrations in Brute-force 90% 

NOx Emissions Reduction CMAQ Simulations to January Monthly Average O3

Concentrations in the 2007 Base CMAQ Simulation. 
8-58 

To better characterize the representativeness of case study areas, paired O3 concentrations and 

population data16 were extracted from each model grid cell and categorized. Figure 8-40 and 

Figure 8-41 depict the percent of U.S. population living in areas with increases or decreases in 

monthly or seasonal mean O3 under the emissions reductions scenarios (50% NOx cut and 90% 

NOx cut respectively) compared to O3 in the base modeling scenario. The top panels show data 

for January monthly mean O3, the center panels show data for seasonal mean O3 (June-August), 

and the bottom panels show data for seasonal mean O3 (April-October). Tabulated results and 

equivalent plots for the combined NOx/VOC cut simulations are provided in Appendix 8C. 

Month by month break-outs for each case study area are also available in Appendix 8C. 

The vast majority of the U.S. population lives in areas where the CMAQ simulations 

predict mean O3 decreases for the June-August and April-October time periods. The majority of 

population living in case-study areas also lives in locations with decreasing seasonal mean O3

concentration under NOx reduction scenarios. As discussed previously, more locations have 

increasing mean O3 in the cooler months as demonstrated by the fact that almost all of the U.S. 

population lives in locations where the model predicts increases in mean O3 in January. The case 

study areas represent 29% of the total U.S. population. These areas account for 20-30% of the 

U.S. population that experience decreasing seasonal mean O3 for April-October in the NOx cut 

simulations and 50-60% of the U.S. population that experience increasing seasonal O3 for AprilOctober. Consequently, the urban study areas over-sample populations living in locations with 

increasing seasonal mean O3 in response to NOx cuts compared to populations living in locations 

with decreases in seasonal mean O3. In all panels displayed in Figure 8-40 and Figure 8-41, most 

of the population lives in locations where increases or decreases in mean O3 were > 1 ppb. 

The proportion of the population living in locations of increasing seasonal mean O3 in 

response to NOx emissions reductions varies considerably between case study areas. Figure 8-42 

and Figure 8-43 show these proportions by city for the 50% and 90% NOx reduction scenarios. 

For the 50% NOx reduction scenario, the CMAQ results predict that four out of fifteen study ares 

(Chicago, Detroit, Los Angeles, and New York) have more than 50% of their populations living 

in locations with increasing mean O3 for April-October. Most other urban study areas have 

between 5% and 30% of their populations living in these areas with increasing mean O3 levels. 

For the 90% NOx reduction scenario, the percent of population living in such locations decreases 

substantially for all cities, leaving four out of fifteen study areas (Detroit, Houston, Los Angeles, 

and New York) with more than 5% of their populations living in areas with increasing mean O3

levels. 

 

16 Block level population data from the 2010 Census was aggregated to the 12km CMAQ grid cell level. The 2007 

population was then calculated using population growth factors developed by Woods and Poole Economics, Inc. 
8-59 

Figure 8-40. Histograms of U.S. Population Living in Locations with Increasing and 

Decreasing Mean O3 Concentrations. Values on the x-axis represent change in mean O3

(ppb) from the 2007 base CMAQ simulation to the 50% NOx cut CMAQ simulation. The 

percentages of the U.S. population living in areas that have changes less than -1 ppb, from -

1 to +1 ppb, and greater than 1 ppb are shown on the y-axis. Left plots show population 

numbers in locations not included in one of the cases study areas while right plots show 

population numbers in locations included in one of the case study areas. Top plots show 

changes in January monthly mean O3, middle plots show changes in seasonal mean JuneAugust O3, and bottom plots show changes in seasonal mean April-October O3. 
8-60 

Figure 8-41. Histograms of U.S. Population Living in Locations with Increasing and 

Decreasing Mean O3 Concentrations. Values on the x-axis represent change in mean O3

(ppb) from the 2007 base CMAQ simulation to the 90% NOx cut CMAQ simulation. The 

percentages of the U.S. population living in areas that have changes less than -1 ppb, from -

1 to +1 ppb, and greater than 1 ppb are shown on the y-axis. Left plots show population 

numbers in locations not included in one of the cases study areas while right plots show 

population numbers in locations included in one of the case study areas. Top plots show 

changes in January monthly mean O3, middle plots show changes in seasonal mean JuneAugust O3, and bottom plots show changes in seasonal mean April-October O3. 
8-61 

Figure 8-42. Population (as % of total case-study area population) Living in Locations of 

Increasing April-October Seasonal Mean O3 in the 50% NOx Reduction CMAQ 

Simulation. 

Figure 8-43. Population (as % of total case-study area population) Living in Locations of 

Increasing April-October Seasonal Mean O3 in the 90% NOx Reduction CMAQ 

Simulation. 

 
8-62 

We can further understand these results by looking at them in terms of population density 

in the case-study areas versus across the U.S. as a whole. As in Section 8.2.3.1, we define census 

tracts with population density greater than 1000 people/km2

 as high population density, but the 

low-mid population density classification used here is a combination of the low and medium 

classifications in that section. Figure 8-44 and Figure 8-45 split out the April-October results 

from Figure 8-40 and Figure 8-41 into high and low-mid sub-categories. Appendix 8C provides 

similar breakouts for the other panels in Figure 8-40 and Figure 8-41. First, based on these 

definitions, we see that 57% of the population in case-study areas lives in high population 

density locations while only 27% of the U.S. population does. As discussed above, the high 

population areas are more likely to experience increases in mean O3 as a result of NOx emission 

reductions compared to lower population areas. Therefore, the fact that the case-study areas used 

in the risk and exposure assessments are more densely populated than the country as a whole 

means that these analyses may estimate higher risks under emissions reduction scenarios than 

would be experienced, on average, across the country. Figure 8-44 and Figure 8-45 show 

generally similar shapes for the high population density histograms in the study-area and nonstudy area locations. In the 50% NOx cut simulation, 69% of the population living in high density 

case-study areas would experience increases in mean seasonal O3 compared to 63% of the 

population the population living in high density areas of the country as a whole. Similarly in the 

90% NOx cut simulation, 28% of the population in high density locations both within the study 

areas and across the U.S. as a whole lives in locations of increasing seasonal mean O3. This 

suggests that the selected study areas adequately represent population-weighted changes in mean 

O3 for people living in high density areas. Similarly, less densely populated locations within the 

case-study areas show O3 increases equivalent to those seen in less densely populated areas in 

the U.S. as a whole. In the 50% NOx cut simulation, 7% of people in low-mid density study area 

locations live where mean seasonal O3 is increasing, while 5% of people in all low-mid density 

U.S. locations live where mean seasonal O3 is increasing. Similarly, in the 90% NOx cut 

simulation, the numbers are 2% for both low-mid density study area populations and for low-mid 

density populations in the U.S. as a whole. Thus the oversampling of populations living in 

locations of increasing mean seasonal O3 in response to NOx cuts, as shown in Figure 8-44 and 

Figure 8-45, appears to be entirely due to the fact that the study areas oversample populations 

living in high density areas compared to the U.S. population as a whole. 
8-63 

Figure 8-44. Histograms of U.S. Population Living in Locations with Increasing and 

Decreasing Mean O3 Concentrations. Values on the x-axis represent the change in seasonal 

mean (April-October) O3 from the 2007 base CMAQ simulation to the 50% NOx cut 

CMAQ simulation. The percentages of the U.S. population living in areas that have 

changes less than -1 ppb, from -1 to +1 ppb, and greater than 1 ppb are shown on the yaxis. Left plots show population numbers in locations not included in one of the cases study 

areas while right plots show population numbers in locations included in one of the urban 

study areas. Bottom plots show histograms for low-mid population density areas while top 

plots show histograms for high population density areas. 
8-64 

Figure 8-45. Histograms of U.S. Population Living in Locations with Increasing and 

Decreasing Mean O3 Concentrations. Values on the x-axis represent the change in seasonal 

mean (April-October) O3 from the 2007 base CMAQ simulation to the 90% NOx cut 

CMAQ simulation. The percentages of the U.S. population living in areas that have 

changes less than -1 ppb, from -1 to +1 ppb, and greater than 1 ppb are shown on the yaxis. Left plots show population numbers in locations not included in one of the cases study 

areas while right plots show population numbers in locations included in one of the urban 

study areas. Bottom plots show histograms for low-mid population density areas while top 

plots show histograms for high population density areas. 
8-65 

8.2.4 Discussion 

We evaluated two different questions, (1) to what degree are the 15 cities evaluated in the 

exposure and risk analyses representative of the overall U.S. population with regards to total O3

risk, and (2) to what degree are they representative of the overall U.S. population with regards to 

the degree of risk reduction that might be observed in response to just meeting the existing and 

alternative standards. 

Regarding the first question, we observe that the 12 urban study areas considered in the 

urban-scale risk assessment presented in Section 7.2 capture urban areas that are among the most 

populated in the U.S., have relatively high O3 levels, and represent the range of city-specific 

effect estimates found by Smith et al. (2009) and Zanobetti and Schwartz (2008). These three 

factors suggest that the urban study areas capture overall risk for the nation well, with a potential 

for better characterization of the high end of the risk distribution. We find that the urban study 

areas are not capturing areas with the highest baseline mortality rates, those with the oldest 

populations, and those with the lowest air conditioning prevalence. These areas tend to have 

relatively low O3 concentrations and low total population, suggesting that the urban study areas 

are not missing high risk populations that have high O3 concentrations in addition to greater 

susceptibility per unit O3. We also find that the 12 urban study areas represent the full range of 

county-level O3-related risk across the entire U.S. We conclude from these analyses that the 12 

urban study areas adequately represent O3-related risk across the U.S. 

Concerning the second question, we observe that the 15 urban areas considered in the 

exposure and risk assessment case study areas over-sample populations living in locations with 

increasing seasonal mean O3 in response to NOx cuts. This suggests that the selected study areas 

adequately represent population-weighted changes in mean O3 concentrations for urban 

populations, but may be under-representing decreasing median O3 concentrations in suburban 

and rural areas. As a result, the risk estimates for populations in the selected urban study areas 

may understate the risk reductions that might be achieved across the broader U.S. population. 

 
8-66 

8.3 REFERENCES 

Abt Associates, Inc. 2010. Model Attainment Test Software (Version 2), prepared for EPA. 

Research Triangle Park, NC: EPA Office of Air and Radiation, Office of Air Quality 

Planning and Standards. Research Triangle Park, NC. 

<http://www.epa.gov/scram001/modelingapps.mats.htm>. 

Abt Associates, Inc. 2010. Environmental Benefits and Mapping Program (Version 4.0), 

prepared for EPA. Research Triangle Park, NC: EPA Office of Air Quality Planning and 

Standards. <http://www.epa.gov/air/benmap>.Anenberg, S.C.; J.J. West; L.W. Horowitz 

and D.Q. Tong. 2010. An estimate of the global burden of anthropogenic ozone and fine 

particulate matter on premature human mortality using atmospheric modeling. 

Environmental Health Perspective. 118:1189-1195. 

Anenberg, S.C.; J.J. West; L.W. Horowitz and D.Q. Tong. 2010. "An Estimate of the Global 

Burden of Anthropogenic Ozone and Fine Particulate Matter on Premature Human 

Mortality Using Atmospheric Modeling." Environmental Health Perspective, 118:1189-

1195. 

Anenberg, S.C.; J.J. West; L.W. Horowitz and D.Q. Tong. 2011. The global burden of air 

pollution mortality: Anenberg et al. respond. Environmental Health Perspective. 

119:A158-A425. 

Bell, M.L.; A. McDermott; S.L. Zeger; J.M. Samet and F. Dominici. 2004. Ozone and short-term 

mortality in 95 U.S. urban communities, 1987-2000. Journal of the American Medical 

Association. 292:2372-2378. 

Byun, D. and K.L. Schere. 2006. Review of governing equations, computational algorithms, and 

other components of the Models-3 Community Multi-scale Air Quality (CMAQ) 

modeling system. Applied Mechanics Reviews. 59:51-77. 

Centers for Disease Control: Wide-ranging Online Data for Epidemiological Research (CDCWonder) (data from years 2004-2006), Centers for Disease Control and Prevention 

(CDC), U.S. Department of Health and Human Services. <http://wonder.cdc.gov>. 

Cooper, O.R.; R. Gao; D. Tarasick; T. Leblanc and C. Sweeney. 2012. Long-term ozone trends 

at rural ozone monitoring sites across the United States, 1990-2010. Journal of 

Geophysical Research. 117(D22), doi:10.1029/2012JD018261. 

Fann N.; A.D. Lamson; S.C. Anenberg; K. Wesson; D. Risley; B.J. Hubbell. 2012. Estimating 

the national public health burden associated with exposure to ambient PM2.5 and ozone. 

Risk Analysis. 32:81-95. 

George, B.J. and T. McCurdy. 2009. Investigating the American Time Use Survey from an 

exposure modeling perspective. Journal of Exposure Science and Environmental 

Epidemiology. 21:92-105. 

Graham, S. and T. McCurdy. 2004. Developing meaningful cohorts for human exposure models. 

Journal of Exposure Analysis and Environmental Epidemiology. 14:23-43. 

Hollman, F.W.; T.J. Mulder and J.E. Kallan. 2000. Methodology and assumptions for the 

population projections of the United States: 1999 to 2100. Population Division Working 

Paper No. 38, Population Projections Branch, Population Division, U.S. Census Bureau, 

Department of Commerce. 
8-67 

Jerrett, M.; R.T. Burnett; C.A. Pope, III; K. Ito; G. Thurston; D. Krewski; Y. Shi; E. Calle; M. 

Thun. 2009. Long-term O3 exposure and mortality. New England Journal of Medicine. 

360:1085-1095. 

Neidell, M. 2009. Information, avoidance behavior and health. J Human Res. 44:450-478. 

Neidell, M. 2010. Air quality warnings and outdoor activities: evidence from Southern California 

using a regression discontinuity approach design. J Epidemiol Community Health. 

64:921-926. 

Samet, J.M.; S.L. Zeger; F. Dominici; F. Curriero; I. Coursac; D.W. Dockery; J. Schwartz and A. 

Zanobetti. 2000. The national morbidity, mortality, and air pollution study part II: 

morbidity and mortality from air pollution in the United States. Health Effects Institute, 

Boston, MA, Number 94, Part II. 

Smith R.L.; B. Xu and P. Switzer. 2009. Reassessing the relationship between ozone and shortterm mortality in U.S. urban communities. Inhalation Toxicology. 21:37-61. 

Timin, B.; K. Wesson and J. Thurman. 2010. Application of model and ambient data fusion 

techniques to predict current and future year PM2.5 concentrations in unmonitored Areas. 

(2010). In Steyn DG, Rao St (eds). Air Pollution Modeling and Its Application XX. 

Netherlands: Springer, pp. 175-179. 

U.S. EPA. 2007. Ozone Population Exposure Analysis for Selected Urban Areas. Research 

Triangle Park, NC: EPA. (EPA document number EPA-452/R-07-010). 

<http://www.epa.gov/ttn/naaqs/standards/ozone/data/2007_07_ozone_exposure_tsd.pdf>. 

U.S. EPA. 2009. Risk and Exposure Assessment to Support the Review of the SO2 Primary 

National Ambient Air Quality Standards: Final Report. Research Triangle Park, NC: 

EPA. (EPA document number EPA-452/R-09-007). 

U.S. EPA. 2010. Quantitative Health Risk Assessment for Particulate Matter. Research Triangle 

Park, NC: EPA. (EPA document number EPA-452/R-10-005). 

U.S. EPA. 2013. Integrated Science Assessment for Ozone and Related Photochemical Oxidants. 

Research Triangle Park, NC: EPA. (EPA document number EPA 600/R-10/076F). 

<http://cfpub.epa.gov/ncea/isa/recordisplay.cfm?deid=247492#Download>.

Woods and Poole Economics Inc. 2012. Complete Demographic Database. Woods and Poole 

Economics, Inc. Washington, DC. <http://www.woodsandpoole.com/index.php.>. 

Zanobetti, A. and J. Schwartz. 2008. Mortality displacement in the association of ozone with 

mortality: an analysis of 48 cities in the United States. American Journal of Respiratory 

and Critical Care Medicine. 177:184-189. 

Zanobetti, A. and J. Schwartz. 2011. Ozone and survival in four cohorts with potentially 

predisposing diseases. American Journal of Respiratory and Critical Care Medicine. 

194:836-841. 

Zhang, L.; D.J. Jacob; N.V. Smith-Downey; D.A. Wood; D. Blewitt; C.C. Carouge; A. van 

Donkelaar; D.B.A. Jones; L.T. Murray and Y. Wang. 2011. Improved estimate of the 

policy-relevant background ozone in the United States using the GEOS-Chem Global 

Model with 1/2°x2/3° horizontal resolution over North America. Atmospheric 

Environment. 45:6769-6776. 

 
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9-1 

9 SUMMARY AND SYNTHESIS 

9.1 INTRODUCTION 

This assessment estimates exposures to O3 and resulting mortality and morbidity health 

risks based on the findings of the O3 ISA (U.S. EPA, 2013) that short-term O3 exposures are 

causally related to respiratory effects, and likely causally related to cardiovascular effects, and 

that long term O3 exposures are likely causally related to respiratory effects. The assessment 

evaluates total exposures and risks associated with the full range of observed O3 concentrations, 

as well as the incremental changes in exposures and risks between just meeting the existing 

standard of 75 ppb and just meeting alternative standard levels of 70, 65, and 60 ppb using the 

form and averaging time of the existing standard: the annual 4th highest daily maximum 8-hr O3

average concentration, averaged over three consecutive years. We evaluated alternative standard 

levels of 70, 65, and 60 consistent with recommendations from CASAC to consider alternative 

standard levels between 60 and 70 ppb (Frey and Samet, 2012). 

Following the conceptual framework described in Chapter 2, the assessment evaluates 

exposures and lung function risk in 15 urban study areas, and mortality and morbidity risks based 

on concentration-response (C-R) functions derived from epidemiology studies in 12 of these 

urban study areas1

. The results from these assessments will help inform consideration of the 

adequacy of the existing primary O3 standards, and potential risk reductions associated with 

several alternative levels of the standard (for the current form and averaging time). In addition, to 

place the urban study area analyses in a broader context, Chapter 8 of this assessment estimates 

the national burden of mortality associated with recent O3 levels, and evaluates the 

representativeness of the 15 urban study areas in characterizing O3 exposures and risks across the 

U.S. This synthesis focuses on the urban study area assessments of exposure and risk for the 

scenarios of just meeting the existing and alternative standards. For this synthesis, we discuss the 

results of the national-scale assessment as they relate to understanding the breadth of O3 risks 

across the U.S. and to the national representativeness of the urban study area risk results. 

To facilitate interpretation of the results of the exposure and risk assessment, this chapter 

provides a synthesis of the various results, focusing on comparing and contrasting those results 

to identify common patterns, or important differences. These comparisons will focus on patterns 

 

1

 Three additional urban study areas were evaluated for the human exposure assessment and lung function risk 

assessment to provide greater geographic representation. There was insufficient information available to conduct 

the epidemiology-based risk assessment in these 3 additional areas. Also, we originally planned to include Seattle, 

WA as a 16th urban study area, but due to limitations in the available air quality monitoring data, we determined 

that it would not be appropriate to model exposure and risks for Seattle (see appendix 4-E). 
9-2 

across urban study areas, across years of analysis, and across alternative standards. In addition, 

factors related to each specific type of analysis that may influence comparisons between the 

analyses are identified and discussed. The degree to which the integrated results are 

representative of national patterns of exposure and risk is evaluated. Overall confidence in the 

results, as well as relative confidence between the different analyses is also assessed. The chapter 

concludes with an overall integrated characterization of exposure and risk in the context of key 

policy-relevant questions raised in Chapter 2. 

9.2 SUMMARY OF KEY RESULTS 

This section provides summaries of key methodological considerations and results from 

each of the major analytical chapters of the Health Risk and Exposure Assessment (HREA). An 

overall summary of the exposure and risk results across urban study areas and alternative 

standard levels is provided in Table 9-1. For human exposures, the results for percent of all 

school-age children experiencing exposures above a particular level of concern are almost 

identical for the percent of asthmatic school-age children experiencing those exposures. In Table 

9-1 and throughout the presentation of summary results, ranges of results across urban study 

areas should be compared between alternative standard levels with the caveat that the ranges for 

the 60 ppb alternative standard level exclude the New York study area, for which we were 

unable to adjust air quality to just meet the alternative standard level. As a result, the ranges may 

not be fully comparable between the alternative standards. 
9-3 

Table 9-1. Summary of Urban Scale O3-Exposure Risk Across Alternative O3 Standard Levels. 

Analysis Metric 

Estimated Risks at Alternative 4th Highest Daily Maximum 8-hr A

70 ppb 65 ppb 

Human Exposure 

% of all school-age children with at least one exposure above 60, 70, or 80 ppb 

Average year 2006-2010 

60 ppb: 3 to 10% 70 ppb: 1% or less 80 ppb: ~0% 

60 ppb: 4% or less 70 ppb: 0.2% or less 80 ppb: 0% 

60 ppb: 70 ppb: 80 ppb: 

Worst case year 2006-2010 

60 ppb: 5 to 19% 70 ppb: 3% or less 80 ppb: 0.2% or less 

60 ppb: <10% 70 ppb: <1% 80 ppb: 0% 

60 ppb: 70 ppb: 80 ppb: 

% of all school-age children with at least two exposures above 60, 70, or 80 ppb 

Average year 2006-2010 

60 ppb: 0.5 to 3.5% 70 ppb: ~0% 80 ppb: 0% 

60 ppb: <1% 70 ppb: 0% 80 ppb: 0% 

60 ppb: 70 ppb: 80 ppb: 

Worst case year 2006-2010 

60 ppb: 1 to 9% 70 ppb: 0.4% or less 80 ppb: 0% 

60 ppb: 3% or less 70 ppb: 0% 80 ppb: 0% 

60 ppb: 70 ppb: 80 ppb: 

Controlled Human Exposure-based Lung Function Risk 

% of all school-age children with at least one occurrence of lung function decrement ≥10%, 15%, or 20% 

Average year 2006-2010 

10% decrement: 11 to 17% 15% decrement: 2 to 4% 20% decrement: 2% or less 

10% decrement: 3 to 15% 15% decrement: 3% or less 20% decrement: <1.5% 

10% dec15% dec20% dec

Worst case year 2006-2010 

10% decrement: 14 to 20% 15% decrement: 3 to 5% 20% decrement: 2% or less 

10% decrement: 4 to 18% 15% decrement: 4% or less 20% decrement: <1.5% 

10% dec15% dec20% dec

% of all school-age children with at least two occurrences of lung function decrement ≥10%, 15%, or 20% 

Average year 2006-2010 

10% decrement: 6 to 11% 15% decrement: 1 to 2.5% 20% decrement: 1% or less 

10% decrement: 1 to 9% 15% decrement: 2% or less 20% decrement: <1% 

10% dec15% dec20% dec

Worst case year 2006-2010 

10% decrement: 7 to 13% 15% decrement: 1 to 3% 20% decrement: 1% or less 

10% decrement: 2 to 11% 15% decrement: 2.5% or less 20% decrement: <1% 

10% dec15% dec20% dec
9-4 

Analysis Metric 

Estimated Risks at Alternative 4th Highest Daily Maximum 8-hr A

70 ppb 65 ppb 

Epidemiologybased Risk 

%/number per 100,000 population of premature deaths from short-term exposures to O3

2007: 0.8 to 3.9% of deaths  2.4 to 17 per 100,000 2009: 0.8 to 3.8% of deaths  2.2 to 16 per 100,000 

2007: 0.8 to 3.2% of deaths  2.3 to 15 per 100,000 2009: 0.8 to 3.3% of deaths  2.2 to 14 per 100,000 

2007: 0. 22009: 0. 2

%/number of per 100,000 population premature respiratoryrelated deaths from long-term exposures to O3

2007: 16 to 20% of deaths  15 to 28 per 100,000 2009: 16 to 20% of deaths  15 to 26 per 100,000 

2007: 13 to 19% of deaths  15 to 26 per 100,000 2009: 14 to 19% of deaths  15 to 25 per 100,000 

2007: 15  15 2009: 15  14 

number of respiratory hospital admissions from short-term exposures to O3

2007: 14 to 190 2009: 15 to 190 

2007: 14 to 150 2009: 15 to 160 

2007: 13 2009: 14 

*Note that the ranges across the urban areas for the 60 ppb alternative standard level excludes the New York study area, for which we wquality to just meet the alternative standard level. As a result, the ranges may not be fully comparable between the alternative standards
9-5 

9.2.1 Air Quality Considerations 

Table 9-2 below gives information on the monitoring network, population, and observed 

peak O3 concentrations for the 15 urban study areas, for the years included in the exposure, lung 

function risk, and epidemiology based risk assessments. The number of counties, number of O3

monitors, population, and design values (DV) are based on the area definitions used in the 

exposure modeling and clinical-based lung function risk assessments, while the 2007 and 2009 

annual 4th highest values are based on the Core Based Statistical Areas (CBSAs) used in the 

epidemiology-based risk assessment. The “N/A” values in the 2007 and 2009 4th high columns 

are for the three urban areas not included in the epidemiology-based risk assessment. The data 

show a trend of lower peak O3 concentrations (i.e., the 2008-2010 design values and 2009 4th

high values are generally lower than the 2006-2008 design values and 2007 4th high values, 

respectively). 

Table 9-2. Area and Monitoring Information for the 15 Urban Study Areas. 

Area Name 

Number 

of 

Counties 

Number 

of O3

Monitors 

Population 

(2010) 

2006-2008 

DV (ppb) 

2007 4th

Highest 

(ppb) 

2008-2010 

DV (ppb) 

2009 4th

Highest 

(ppb)

Atlanta 33 13 5,618,431 95 102 80 77 

Baltimore 7 7 2,710,489 91 92 89 83 

Boston 10 14 5,723,468 83 89 77 75 

Chicago 16 26 9,686,021 78 N/A 74 N/A 

Cleveland 8 13 2,881,937 82 83 77 72 

Dallas 11 20 6,366,542 89 N/A 86 N/A 

Denver 13 26 3,390,504 86 97 77 79 

Detroit 9 12 5,218,852 81 93 75 73 

Houston 10 22 5,946,800 91 90 85 91 

Los Angeles 5 54 17,877,006 119 105 112 108 

New York 27 31 21,056,173 90 94 84 81 

Philadelphia 15 19 7,070,622 92 102 83 74 

Sacramento 7 26 2,755,972 102 93 102 96 

St. Louis 17 17 2,837,592 85 94 77 74 

Washington 26 22 5,838,518 87 N/A 81 N/A 

In this analysis, we employed a photochemical model-based adjustment methodology 

Simon et al. (2013) using the Higher-Order Decoupled Direct Method (HDDM) capabilities in 

the Community Multi-scale Air Quality Model (CMAQ) (hereafter referred to as HDDM air 
9-6 

quality adjustment). The HDDM air quality adjustment methodology replaced the quadratic 

rollback technique used in the first draft HREA to estimate O3 concentrations consistent with just 

meeting existing and alternative O3 standards. The HDDM air quality adjustment procedure 

estimates the change in observed hourly O3 concentrations at a given set of monitoring sites 

resulting from national across-the-board reductions in U.S. anthropogenic NOx and/or VOC 

emissions. In this analysis, we adjusted O3 concentrations to just meet the existing standard of 75 

ppb2 and potential alternative standards of 70, 65, and 60 ppb at ambient monitoring sites in the 

15 urban study areas for the 2006-2008 and 2008-2010 periods. In most locations, only NOx

reductions were used to adjust the distribution of O3 concentrations, because of the 

ineffectiveness of VOC reductions in reducing peak O3 concentrations needed to meet the 

existing and alternative standard levels. Sensitivity analyses were also conducted in some 

locations to evaluate the impact of decreasing both NOx and VOC emissions. 

The HDDM air quality adjustment methodology represents a substantial improvement 

over the quadratic rollback method used to adjust O3 concentrations in previous reviews. First, 

quadratic rollback was a purely mathematical technique which attempted to reproduce the 

distribution of observed O3 concentrations just meeting various standards, while the new 

methodology uses photochemical modeling to simulate the response in O3 concentrations due to 

changes in precursor emissions based on current understanding of atmospheric chemistry and 

transport. Second, quadratic rollback used the same mathematical formula to adjust 

concentrations at all monitors within each urban study area for all hours, while HDDM allows 

the adjustments to vary both spatially across each urban study area and temporally across hours 

of the day and across seasons. Finally, quadratic rollback was designed to only allow decreases 

in O3 concentrations, while the HDDM air quality adjustment allows both increases and 

decreases in O3 concentrations in response to reductions in NOx or VOC emissions. For example, 

in response to reductions in NOx emissions, the HDDM methodology is able to capture increases 

in O3 concentrations that can occur in urban cores characterized by titration of O3 by fresh NO 

emissions and decreases in O3 concentrations downwind. In addition, the HDDM methodology 

removes the need to assume a particular “floor” of background ozone concentrations, as the fully 

characterized chemistry in the model accounts for both anthropogenic emissions (domestic and 

international) and natural emission sources, and we are able to focus emissions reductions on 

U.S. anthropogenic emissions alone in adjusting O3 concentrations to just meet existing and 

alternative O3 standard levels. 

 

2

 Just meeting the existing standard level of 75ppb is determined by the 4th highest daily maximum 8-hr average O3

concentration, averaged over 3 years (hereafter referred to as the existing standard). 
9-7 

Following HDDM adjustment of O3 concentrations, several general trends are evident in 

the changes in O3 patterns across the urban study areas and across the alternative standard levels. 

In all 15 urban study areas, peak O3 concentrations tended to decrease while the O3

concentrations in the lower part of the distribution of O3 tended to increase as the concentrations 

were adjusted to meet the existing and alternative standards. In addition, O3 concentrations in the 

high and mid-range portions of the O3 distribution generally decreased in the outer, more rural 

and suburban portions of the urban study areas, while the O3 response to NOx reductions was 

more varied within the urban cores. In particular, while the peak (annual 4th highest daily 

maximum 8-hr average) concentrations upon which the existing and alternative standards are 

defined generally decreased in the urban core of the urban study areas in response to modeled 

reductions in primarily NOx emissions, the O3 responses near the center of the O3 distribution at 

these locations followed one of three patterns when focusing on the mean of the daily maximum 

8-hr O3 concentrations from May to September, as shown in Table 9-3. 

Table 9-3. General Patterns in Seasonal (May-Sept) Mean of Daily Maximum 8-hr O3

Concentrations after Adjusting to Meet Existing and Alternative Standards.* 

After Adjusting Air Quality to 

Just Meet Existing Standard 

After Further Adjusting to Just Meet 

Lower Alternative Standards 

Urban Study Areas 

Showing Pattern 

Decreased Continued to decrease Atlanta, Sacramento 

Washington, D.C 

Increased Decreased 

Baltimore, Cleveland 

Dallas, Detroit, Los 

Angeles. New York 

Philadelphia, St. Louis 

Increased Continued to increase or remained 

constant 

Boston, Chicago, 

Denver, Houston 

* These patterns refer to O3 responses in the urban core of each urban study area based on analysis of the 

interpolated monitor values used as inputs to the exposure and lung function risk analyses.

The air quality inputs to the exposure modeling and clinical-based lung function risk 

assessments were estimated hourly O3 concentrations at each census tract in the 15 urban study 

areas. These values were interpolated from the observed and HDDM-adjusted monitoring data 

using the Voronoi Neighbor Averaging (VNA) technique. This technique was shown to be an 

improvement upon the nearest neighbor technique used in the first draft HREA and previous O3

NAAQS reviews (see Appendix 4-A for details). Consequently, the spatial variability of 

observed and HDDM-adjusted O3 is better accounted for in these analyses compared to those in 

the first draft HREA. 

The air quality inputs to the epidemiology based risk assessment were “composite 

monitor” values, a time-series of the spatially averaged monitoring data, in 12 of the 15 urban 

study areas. Consequently, in cases of urban study areas within which O3 was predicted to 
9-8 

increase in some locations and decrease in others, the air quality inputs to this analysis represent 

a “net” effect for each urban study area. The spatial extent of the urban study areas used in the 

composite monitor averages were CBSAs. These CBSA areas are larger than the Zanobetti and 

Schwartz, 2008 (Z & S) study areas (used in the first draft HREA) which include only a subset of 

the CBSA focused on urban cores. Figure 9-1 (reproduced from Figure 4-7) shows box plots of 

the composite monitor values for 2006-2008 based on the observed data (black), data adjusted to 

meet the existing standard using quadratic rollback (blue), and the HDDM adjustment procedure 

(red) for the Z & S areas. The two adjustment methods were generally comparable in terms of 

the changes in the upper quartile of the distribution. However, by design, quadratic rollback 

always estimated decreases in the 75th percentile, median, and 25th percentile of the composite 

monitor values, while HDDM estimated decreases in these values in some urban study areas, and 

increases in other areas consistent with atmospheric chemistry. HDDM-based adjustments 

always produced increases in the lower tail of the distribution, while the lower tail values 

generally remained unchanged with quadratic rollback. The differences between the two 

adjustment procedures were the most pronounced in Los Angeles and New York, where the 

largest reductions in NOx were required in order to meet the existing and alternative standards. 

These large reductions in NOx caused a relatively large increase in lower O3 concentrations 

because of the reduction in NOx titration of O3. As was noted in Chapter 4, the HDDM-based O3

estimates become more uncertain for larger changes in NOx and VOC emissions, and thus there 

was less overall confidence in those results. Even in these cases, the HDDM approach is still 

preferable because it captures better the overall shift in the distribution of O3 concentrations. 
9-9 

Figure 9-1. Distributions of Composite Monitor Daily Maximum 8-hr Average O3

Concentrations from Ambient Measurements (black), Quadratic Rollback (blue), and the 

HDDM Adjustment Methodology (red) Used for Just Meeting the Existing O3 Standard. 
9-10 

9.2.2 Human Exposure Modeling 

The population exposure assessment evaluates exposures to O3 using the Air Pollution 

Exposure (APEX) model for the general population, all school-age children (ages 5-18), 

asthmatic school-age children (ages 5-18), asthmatic adults (ages > 18), and older adults (ages 65 

and older), with a focus on populations engaged in moderate or greater exertion (e.g. children 

engaged in outdoor recreational activities). The strong emphasis on children, asthmatics, and 

older adults reflected the findings of the last O3 NAAQS review (U.S. EPA, 2007) and the ISA 

(U.S. EPA, 2013, Chapter 8) that these are important at-risk groups. 

We assessed exposure in 15 urban study areas – Atlanta, Baltimore, Boston, Chicago, 

Cleveland, Dallas, Denver, Detroit, Houston, Los Angeles, New York, Philadelphia, Sacramento, 

St. Louis, and Washington, D.C. – for recent O3 concentrations (2006-2010) and for O3

concentrations adjusted to just meet the existing 8-hr O3 standard (75 ppb) and alternative 

standard levels of 70, 65, 60 ppb3

 for two time periods (2006-2008 and 2008-2010)4. The 

analysis provided estimates of the percent of several study groups of interest exposed to 

concentrations at or above three controlled human exposure-based 8-hr average O3 exposure 

benchmarks: 60, 70, and 80 ppb. The ISA includes studies showing statistically significant 

effects at each of these benchmark levels (U.S. EPA, 2013). These benchmarks were selected to 

provide some perspective on the public health impacts from exposures to various concentrations 

that have been associated with O3-related health effects (e.g., lung inflammation and increased 

airway responsiveness) in controlled human exposure and toxicological studies, but cannot 

currently be evaluated in quantitative risk assessments. In addition, the exposure assessment also 

identified the specific microenvironments and activities that contribute most to exposure and 

evaluated at what times and how long individuals were in key microenvironments and were 

engaged in key activities. This assessment focused on persons experiencing the highest daily 

maximum 8-hr exposure within each study area. The assessment found that: 

• Childhood is an important lifestage where higher exposures and risks can occur, due 

to the higher time spent outdoors by children, the higher exposure concentration 

 

3

 We were not able to adjust air quality to just meet the 60 ppb alternative standard in the New York study area by 

reducing U.S. NOx and VOC emissions (see chapter3 and appendix 4-D for details). Detroit was already meeting 

the existing standard for 2008-2010. 4

 Just meeting the O3 standard is based on the 4th highest daily maximum 8-hr average O3 concentration, averaged 

over 3 years. We evaluated two different 3-year periods in determining how air quality in each of the analytical 

years would respond to just meeting the existing and alterative levels of the standard. This was done to evaluate 

the effect of variability in meteorology and emissions on exposures and risks associated with just meeting the 

existing and alternative standards. For the exposure and lung function risk analyses, which provide estimates for 

each of the five analytical years, this results in two estimates for 2008, because 2008 is included in each of the 3-

year averaging periods and there are separate analytical results for 2008 for the adjusted air quality resulting from 

simulating just meeting the standard in each of the two 3-year periods. 
9-11 

experienced by children while outdoors (i.e. when they are dismissed from school in 

the afternoon and during the summer, when they may be at an outdoor camp all day) 

and engagement in moderate or high exertion level activities. 

• Persons spending a large portion of their time outdoors during afternoon hours 

experienced the highest 8-hr average O3 exposure concentrations given that O3

concentrations in other microenvironments were simulated to be lower than ambient 

concentrations. 

• Highly exposed children spend half of their outdoor time (on average) engaged in 

moderate or greater exertion levels, such as in sporting activities. Highly exposed 

adults also spent their outdoor time engaged in moderate or greater exertion levels 

though on average, not as frequently as children. 

Across the 15 urban study areas, we find that school-age children are of greatest concern 

for O3 exposures compared to other lifestages due to the greater amount of time they spend 

outdoors engaged in moderate or higher exertion activities. The exposure analysis estimates that 

school-age children have the highest percent of exposures of concern of any of the at-risk 

populations or lifestages. As a result, we focus on the results for school-age children (ages 5-18) 

in the remainder of this discussion. Figure 9-2 (reproduced from Figure 5-5) shows the results of 

the exposure assessment for all 15 urban study areas, showing trends across the analytical years 

for the percent of all school-age children with at least one daily maximum 8-hr average O3

exposure at or above the 60, 70, and 80 ppb benchmarks. 

The limited availability of longitudinal activity diary data and the general population 

modeling approach used may underestimate the correlation in activity patterns for certain 

susceptible populations (e.g., outdoor workers), and underestimate how often there are repeated 

exposures to O3 concentrations above the exposure benchmarks. As a result, although we are 

able to report the percent of the population with at least one exposure greater than the alternative 

exposure benchmarks, we are less confident in the estimated percent of the population 

experiencing more than one exposure. Individuals with repeated exposures may be at greater risk 

of significant health effects (U.S. EPA, 2013, Section 6.2.1.1). In addition, the limited data on 

responses to air quality alerts (e.g., averting behavior) indicates that a small percentage of the 

population may engage in averting behavior in response to air pollution, which may overstate 

actual exposures if individuals reduce their exposure during periods of high O3. 

The benchmark exposures of concern are not equivalent to ambient standard levels, as 

exposures reflect the full pattern of O3 concentrations throughout a season, coupled with time 

spent outdoors and indoors engaged in different activities. Thus, just meeting the existing 

standard will result in shifts in the entire distribution of O3 over a three year period, and will 

change the percent of populations experiencing each of the exposure benchmarks of concern. 
9-12 

Figure 9-2 shows that the percent of all school-age children at or above the 60 ppb exposure 

benchmark declines consistently across the 15 urban study areas when just meeting potential 

alternative standards of 70, 65, and 60. For most urban study areas and years, the percent of all 

school-age children at or above the 60 ppb exposure benchmark is reduced by over half when O3

is adjusted to meet the 65 ppb alternative standard relative to the 75 ppb standard. In many urban 

study areas and years, just meeting the 65 ppb alternative standard results in close to zero percent 

of all school-age children above the 60 ppb benchmark. For the 70 and 80 ppb benchmarks, 

meeting an alternative standard of 70 ppb results in a small percentage of all school-age children 

exceeding the exposure benchmarks. 

Year-to-year variability is relatively pronounced for exceedances of the 60 ppb 

benchmark. In addition, we observe a geographic pattern to the years with the maximum percent 

of exceedances of the exposure benchmarks reflecting the regional O3 patterns across years. In 

general, northeastern urban study areas saw the highest percentage of benchmark exceedances 

during 2007, while southern and western urban study areas saw a higher percentage of 

benchmark exceedances during 2006. However, these patterns are somewhat dependent on the 3-

year averaging period used to determine whether the standards are met. In general variability in 

the percent of all school-age children exceeding the 60 ppb exposure benchmark across urban 

study areas is similar to the variability across years. 

The percent of all school-age children with multiple exposures above the exposure 

benchmarks is generally much lower compared to the percent of all school-age children with 

single exposures above the benchmarks. However, as noted above, we have lower confidence in 

these estimates. Even for the lowest benchmark level of 60 ppb, most locations and years have 

less than 10 percent of all school-age children experiencing 2 or more exposures when just 

meeting the existing standard of 75 ppb, less than 5 percent when just meeting an alternative 

standard of 70 ppb, and less than 1 percent when just meeting an alternative standard of 65 ppb. 

For most urban study areas and years, less than 1 percent of all school-age children experience 2 

or more exposures at or above the 70 ppb exposure benchmark when just meeting the existing 

standard. 
9-13 

Figure 9-2. Effect of Just Meeting Existing (column 1) and Alternative (columns 2 through 

4) Standards on the Percent of All School-age Children (ages 5-18) with at Least One Daily 

Maximum 8-hr O3 Exposure at or above 60, 70, and 80 ppb while at Moderate or Greater 

Exertion, 2006-2010 Air Quality. Percent of All School-Age Children with at Least One 8-hour Exposure At or Above Benchmark Level While at Moderate or Greater Exertion, Adjusted Air Qualit

y
9-14 

Table 5-11 summarized the percent of the all school-age children (ages 5-18) with at least 

one daily 8-hr exposure above the 60, 70, and 80 ppb benchmarks, providing both the mean and 

maximum percentage across the five analytical years for each urban study area. For O3 adjusted 

to just meet the existing standard of 75 ppb, the highest maximum percentage of all school-age 

children exceeding the 60 ppb benchmark across years, 26 percent, occurs in Denver and St. 

Louis, both study areas also having the highest mean percentage averaged across years (about 

16-17%). After just meeting the existing standard, Los Angeles has the lowest maximum (10 

percent) and mean (9.5 percent) percentage of all school-age children exceeding the 60 ppb 

benchmark across years, likely reflecting the highly skewed nature of O3 concentrations in that 

urban study area. For example, just meeting the existing standards in Los Angeles moves the 

majority of O3 concentrations (sites and days) well below 60 ppb (See Appendix 4-D). Patterns 

across urban study areas are generally similar after just meeting alternative standards of 70, 65, 

and 60 ppb, with the exception that the lowest maximum and mean percentage of all school-age 

children for the alternative standard level of 65 ppb occurs in the New York urban study area, 

which had very large (greater than 90 percent) reductions in NOx emissions that were used to 

adjust air quality to just meet the 65 ppb standard level in that urban study area. This resulted in 

the distribution of O3 concentrations covering most days of the year and most monitoring sites 

shifting dramatically downward, with most concentrations well below 60 ppb across the New 

York urban study area. The level of confidence in the results for the New York and Los Angeles 

urban study areas for just meeting the alternative standards is lower than that for some of the 

other urban study areas due to the HDDM-based O3 estimates becoming more uncertain for very 

large changes in precursor emissions. 

Figure 9-3 (reproduced from Figure 5-25) presents the results of the exposure assessment 

for all 15 urban study areas, showing the effect on the percent of all school-age children with one 

or more exposures above the 60 ppb benchmark of just meeting the existing and alternative 

standards. For each alternative standard, Figure 9-3 shows the maximum percent of all schoolage children exceeding the benchmark across the modeled years 2006-2010. Patterns of results 

are similar for the 70 ppb and 80 ppb benchmarks, however, the maximum percents of all schoolage children exceeding those higher benchmarks are much smaller for all alternative standards. 

The percent of all school-age children exceeding the 80 ppb benchmark is close to zero once the 

existing standard is met. The percent of all school-age children with two or more exposures 

exceeding the 60 ppb benchmark level is substantially lower when just meeting the existing 

standard, and is close to zero for the 70 ppb and 80 ppb benchmarks. This percentage drops 

substantially when meeting the 70 ppb standard, and is close to zero in most urban study areas 

when meeting the 65 ppb and 60 ppb alternative standards. Patterns for asthmatic school-age 

children are very similar to patterns for all school-age children. 
9-15 

Figure 9-3. Effect of Just Meeting the Existing (75 ppb) and Alternative Standards on the 

Percent of All School-age Children (ages 5-18) at or above the 60 ppb Exposure 

Benchmark, Maximum Value Across All Years in Each Study Area, 2006-2010 Air Quality. 

9.2.3 Health Risks Based on Controlled Human Exposure Studies 

Using the estimates of exposure from APEX combined with results from controlled 

human exposure studies, we estimated the number and percent of at-risk populations or lifestages 

(all school-age children ages 5-18, children with asthma ages 5-18, adults ages 18-35, adults ages 

36-55, and outdoor workers) experiencing selected decrements in lung function. The analysis 

focuses on estimates of the percent of each at-risk population or lifestage experiencing a 

reduction in lung function (mostly for durations of one to five hours) for three different levels of 

impact, 10, 15, and 20 percent decrements in forced expiratory volume in one second (FEV1). 

These levels of impact were selected based on the literature discussing the adversity associated 

with increasing lung function decrements (US EPA, 2013, Section 6.2.1.1). Consistent with the 

exposure assessment, we focus this summary on lung function decrements in children as they are 

the lifestage likely to have the greatest percentage at-risk due to higher levels of exposure and 

exertion. Within the overall population of children, asthmatic children may have less reserve 

lung capacity to draw upon when faced with decrements, and therefore a ≥10 percent decrement 

in lung function may be a more adverse event in an asthmatic child than a healthy child. 

Lung function risks (based on experiencing a 10, 15, or 20 percent decrement in lung 

function) were estimated in each of the 15 urban study areas. Two methods were used to estimate 
9-16 

lung function risks: one based on application of a population level exposure-response (E-R) 

function consistent with the approach used in the 2008 O3 NAAQS review, and one based on 

application of an individual level E-R function introduced in this review (the McDonnellStewart-Smith (MSS) model) that incorporates individual differences in physiology, age, and 

activity patterns (McDonnell et al., 2012) as well as accounting for the full distribution of 

exposures, not simply the maximum. Because the individual level E-R function approach allows 

for a more complete estimate of risk (incorporating risk responses at varying activity levels, not 

just moderate or greater exertion), we focus on the results of that approach here. 

The MSS model as implemented in APEX has a variable that adjusts the lung function 

response according to an individual's age. The MSS model was fit using data from subjects who 

ranged in age from 18 to 35. Thus, the MSS model is not able to account for differences in lung 

function at different age groups between the ages of 5 and 18. However, age does have a 

pronounced effect on lung function response in the APEX model. APEX models differences in 

physiological parameters due to age, and these result in age-dependent predictions of ventilation 

rates, which are used in the MSS model. Ventilation rates also depend on the activities being 

performed, which are also age-dependent. As a result of differences in physiology and activities, 

the lung function responses vary by age (see Appendix 6-E). 

Figure 9-4 (reproduced from Figure 6-7) shows the results of the lung function risk 

assessment for all 15 urban study areas, showing trends across the analytical years for the percent 

of children with predicted lung function decrements greater than or equal to 10 percent5

. 

Specifically, Figure 9-4 shows that the percent of children (age 5-18) with greater than or equal 

to 10 percent lung function decrement declines consistently across the 15 urban study areas when 

just meeting the existing 75 ppb standard, as well as the alternative standards of 70, 65, and 60. 

The percent of children at-risk at the 10 percent decrement level remains at or above 10 percent 

in many locations after just meeting the 60 ppb alternative standard. The percentage of children 

with greater than or equal to a 15 or 20 percent lung function decrement is much lower for all 

alternative standards, with close to zero percent of children at-risk when just meeting the 

alternative standard of 60 ppb. In general variability in percent of children at-risk across urban 

study areas is similar to variability across years. 

 

5

 We introduced this new method (relative to the 2008 O3 NAAQS review) for calculating the percent of the at-risk 

study groups experiencing lung function decrements, based on modeling individual level responses to O3

exposures. This new method yields higher estimates of the percent of children experiencing lung function 

decrements greater than 10, 15, and 20 percent. This may be partly due to the specific data inputs from clinical 

studies used to derive the function, but is also to be expected because the new MSS model can reflect greater 

sensitivity of children to O3 exposures because it allows for age variability in the relationship between O3 and 

FEV1 decrements, and younger people are more responsive to O3 exposures than older people. 
9-17 

Figure 9-4. Effect of Just Meeting the Existing (column 1) and Alternative (columns 2-4) 

Standards on the Percent of All School-age Children with FEV1 decrements > 10, 15, and 

20%, 2006-2010 Air Quality. Percent of All School-age Children with at Least One FEV1 Decrement 

≥ 10% 
9-18 

Figure 9-5 (reproduced from Figure 6-13) shows the results of the lung function risk 

assessment for all 15 urban study areas, showing the effect on the risk of a 10 percent or greater 

lung function decrement in children (ages 5-18) of just meeting the existing and alternative O3

standards. For each alternative standard, Figure 9-5 shows the maximum percent risk over all of 

the modeled years 2006-2010. 

There is no consistent pattern in the percent of children with 10 percent or greater lung 

function decrement across urban study areas just meeting the existing standard of 75 ppb. The 5-

year maximum estimated percent of children at-risk ranges from 17 to 22 percent across urban 

study areas. The percent reduction in 5-year maximum risk when just meeting the 70 ppb 

alternative standard is more consistent across urban study areas, ranging from 8 to 23 percent 

(excluding the New York study area, which had a reduction of 29 percent). Reductions in risk 

when just meeting the 65 ppb alternative standard are also generally consistent across urban 

study areas, with the exception of the New York study area. Incremental reductions in risk when 

just meeting the alternative 65 ppb standard compared with just meeting the 70 ppb alternative 

standard range from 17 to 31 percent excluding the New York study area, which has a reduction 

in risk of more than twice as much as the next largest reduction. Incremental reductions in risk 

from just meeting the alternative 60 ppb standard compared with just meeting the 65 ppb 

standard are generally consistent, ranging from 16 to 46 percent, with somewhat larger 

reductions in risk occurring in Cleveland and Denver. Overall, the 5-year maximum percent of 

children at-risk for lung function decrements of 10 percent or more exceeds 13 percent, 10 

percent, and 5 percent in all urban study areas except New York after just meeting alternative 

standards of 70, 65, and 60, respectively. Patterns of risk reductions are also similar for the 

alternative lung function decrement levels of 15 percent and 20 percent. However, the initial 

percent of the population experiencing these decrements when just meeting the existing standard 

are substantially lower. 

Patterns of risk responses using the population level E-R model are similar to the MSS 

individual risk model. However, the starting values for the percent of the population at risk are 

lower, reflecting the limits of the model in reflecting individual level responses, and the limited 

coverage of the model for exposures at lower exertion levels. For children, the MSS model gives 

results typically a factor of three higher than the population level E-R model used in the previous 

O3 NAAQS review. 
9-19 

Figure 9-5. Effect of Just Meeting Existing (75 ppb) and Alternative Standards on the 

Percent of All School-age Children (ages 5-18) with FEV1 Decrements ≥ 10%, Maximum 

Value for Each Urban Study Area, 2006-2010 Air Quality. 

9.2.4 Health Risks Based on Epidemiological Studies (Chapters 7 and 8) 

The epidemiology-based risk assessment evaluated mortality and morbidity risks from 

short-term O3 exposures and mortality risks from long-term exposures to O3 by applying C-R 

functions derived from selected epidemiology studies. The analysis included both a set of urban 

scale analyses and a national-scale assessment. The urban study analyses evaluated mortality and 

emergency department (ED) visits, hospitalizations, and respiratory symptoms associated with 

recent O3 concentrations (2006-2010) and with O3 concentrations adjusted to just meet the 

existing and alternative O3 standards (see section 9.2.1 and Chapter 4). Mortality and hospital 

admissions (HA) were evaluated in 12 urban study areas, while ED visits and respiratory 

symptoms were evaluated in a subset of areas with supporting epidemiology studies. The 12 

urban study areas were: Atlanta, GA; Baltimore, MD; Boston, MA; Cleveland, OH; Denver, CO; 

Detroit, MI; Houston, TX; Los Angeles, CA; New York, NY; Philadelphia, PA; Sacramento, 

CA; and St. Louis, MO. The urban study analyses focus on risk estimates for the middle year of 

each three-year design value period (2006-2008 and 2008-2010) in order to provide estimates of 

risk for a year with generally higher O3 concentrations (2007) and a year with generally lower O3

concentrations (2009). 

standard level (ppb) 60 65 70 75

Washington

St Louis

Sacramento

Philadelphia

New York

Los Angeles

Houston

Detroit

Denver

Dallas

Cleveland

Chicago

Boston

Baltimore

Atlanta

percent of school-aged children with FEV1 decrement > 10%

0% 2% 4% 6% 8% 10% 12% 14% 16% 18% 20%
9-20 

Most of the endpoints evaluated in epidemiology studies cover the entire study 

population including children and adults. Because most mortality and hospitalizations occur in 

older persons, these epidemiology-based risk estimates are better indicators of effects in adults 

than in children. This is an important distinction from the human exposure and lung function risk 

assessments, which focus on children. The only endpoints specific to children are asthma and all 

respiratory hospital admissions using the New York specific epidemiology study, respiratory ER 

visits in Atlanta, and respiratory symptoms in asthmatic children in Boston. 

Both the urban study area and national-scale assessments provide the absolute incidence 

and percent of incidence attributable to O3. In addition, risks are presented in terms of incidence 

per 100,000 population to control for the differences in the sizes of the populations across urban 

study areas, and to allow for comparison of risks using different definitions of urban extent. In 

previous reviews, O3 risks have only been estimated for the portion of total O3 attributable to 

North American anthropogenic sources (above what was referred to in previous reviews as 

“policy-relevant background O3”). In contrast, this assessment estimates risk for O3

concentrations down to zero, reflecting the lack of evidence for a detectable threshold in the C-R 

functions (U.S. EPA, 2013, Chapter 2), and the understanding that U.S. populations may 

experience health risks associated with O3 resulting from emissions from all sources, both natural 

and anthropogenic, within and outside the U.S. In order to better reflect how O3 distributions are 

likely to respond to just meeting existing and potential alternative standard levels, we adjusted 

O3 concentrations to just meet existing and potential alternative standard levels using reductions 

in only U.S. anthropogenic emissions of O3 precursors. Thus, the estimated changes in risk 

between just meeting the existing standards and just meeting potential alternative standard levels 

only reflect reductions in U.S. anthropogenic emissions. 

However, consistent with the conclusions in the O3 ISA (U.S. EPA, 2013), we have 

relatively lower certainty about the shape of the C-R function towards the lower end of the 

distribution of O3 concentrations used in fitting the function due to the reduction in the number 

of O3 measurements in this portion of the distribution. We discuss this source of uncertainty 

below. In addition, we provide the distribution of mortality incidence across the range of O3

concentrations in Chapter 7 to inform discussions of uncertainty in the results. 

9.2.4.1 Urban study area results 

Figure 9-6 (reproduced from Figures 7-4 and 7-5) show the results of the mortality and 

adult (ages 65 and older) respiratory hospital admissions risk assessments for all 12 urban study 

areas, showing the effect on the incidence per 100,000 population just meeting the existing 75 

ppb standard and alternative O3 standards of 70, 65, and 60 ppb in 2007 and 2009. 
9-21 

Figure 9-6. Effect of Just Meeting Existing (75 ppb) and Alternative Standard Levels on Mortality Risk p

Population (left panels) and on Adult (ages 65 and older) Respiratory Hospital Admissions Risk per 100,00(top panels) and 2009 (bottom panels) Air Quality.

2007 Simulation year

2009 Simulation year

02468

101214161820

75ppb 70ppb 65ppb 60ppb

Total ozone‐related mortality per 100,000 residents

Trend in ozone‐related mortality across standard

levels (deaths per 100,000)

Atlanta, GABaltimore, MDBoston, MACleveland, OHDenver, CODetroit, MIHouston, TXLos Angeles, CANew York, NYPhiladelphia, PASacramento, CASt. Louis, MO

02468

101214161820

75ppb 70ppb 65ppb 60ppb

Total ozone‐related mortality per 100,000 residents

Trend in ozone‐related mortality across standard levels

(deaths per 100,000)

Atlanta, GABaltimore, MDBoston, MACleveland, OHDenver, CODetroit, MIHouston, TXLos Angeles, CANew York, NYPhiladelphia, PASacramento, CASt. Louis, MO

2007 Simulation year

2009 Simulation year

468

10121416

75ppb 70ppb 65ppb 60ppb

Total ozone‐related HA per 100,000

Trend in ozone‐related HA across standard 

(HA per 100,000)

468

10121416

75ppb 70ppb 65ppb 60ppb

Total ozone‐related HA per 100,000

Trend in ozone‐related HA across standard 

(HA per 100,000)
9-22 

In some urban study areas which have large NOx emissions (e.g. from heavy downtown 

traffic), O3 levels are artificially low because the NOx emissions remove O3 through chemical 

reactions (see section 9.2.1 and Chapter 4). In these places, when NOx emissions are decreased to 

reduce peak O3 concentrations across the entire CBSA, which often includes locations outside of 

the urban core areas, lower concentrations of O3 can go up. This can also happen in other areas 

on the lowest O3 days. This phenomenon occurs in some locations when meeting lower 

alternative standards as well. 

The overall trend across urban study areas is small decreases in mortality and morbidity 

risk as O3 concentrations are adjusted to just meet incrementally lower alternative standard 

levels. In New York, there are somewhat greater decreases in these risks, reflecting the relatively 

large emission reductions used to adjust air quality to just meet the 65 ppb alternative standard, 

and the substantial change in the distribution of O3 concentrations that resulted. We were not 

able to adjust O3 concentrations to just meet the 60 ppb alternative standard in the New York 

urban study area. Risks vary substantially across urban study areas; however, the general pattern 

of reductions across the alternative standards is similar between urban study areas. Because of 

the generally lower baseline O3 concentrations in 2009, risks are generally slightly lower in 2009 

relative to 2007; however, the patterns of reductions in risk are very similar between the two 

years. 

Compared with exposures of concern and lung function risks, mortality and morbidity 

risks based on epidemiology studies generally do not show as large responses to meeting existing 

or alternative levels of the standard for several reasons. First, these risks are based on C-R 

functions that are approximately linear along the full range of concentrations, and therefore 

reflect the impact of changes in O3 along the complete range of 8-hr average O3 concentrations. 

This includes days with low baseline6

 O3 concentrations that are predicted to have increases in 

O3 concentrations, as well as days with higher starting O3 concentrations that are predicted to 

have decreases in O3 concentrations as a result of just meeting existing and alternative standards. 

Second, these risks reflect changes in the urban-area wide monitor average, which will not be as 

responsive to air quality adjustments as the design value monitor, and which includes monitors 

with both decreases and increases in 8-hr concentrations. Third, the days and locations with 

predicted increases in O3 concentrations (generally those with low to midrange starting O3

concentrations) resulting from just meeting the existing or alternative standard levels generally 

are frequent enough to offset days and locations with predicted decreases in O3. The heat maps 

presented in Figures 7-2 and 7-3 demonstrate that just meeting progressively lower alternative 

 

6

 By low baseline concentrations, we mean area-wide average O3 concentrations between approximately 10 and 40 

ppb prior to adjustments to just meet the existing and alternative standards. 
9-23 

standard levels narrows the distribution of risk across the range of O3 concentrations. In addition, 

the distribution of risk tends to be more centered on area-wide average concentrations in the 

range of 25 to 55 ppb after just meeting an alternative standard of 60 ppb. The focus of the 

epidemiological studies on urban study area-wide average O3 concentrations, and the lack of 

thresholds coupled with the linear nature of the C-R functions mean that in this analysis, the 

impact of a peak-based standard (which seeks to reduce peak concentrations regardless of effects 

on low or mean concentrations) on estimates of mortality and morbidity risks based on results of 

those studies is relatively small. For example, for mortality and hospital admissions (based on 

applying C-R functions from the Medina-Ramon et al multicity study), we find a less than or 

equal to 5, 10, and 17 percent reduction in risk for most urban study areas (excluding New York) 

when just meeting the 70 ppb, 65 ppb, and 60 ppb alternative standards, respectively, compared 

to just meeting the existing standard. The general pattern for other morbidity risks is similar to 

hospital admissions. However, we are not able to draw strong conclusions about the results 

across urban study areas, because of the limited number of urban study areas represented for 

most of the endpoints. 

We have applied city-specific mortality effect estimates to each urban study area based 

on the largest multi-city epidemiological study. However, for many of the urban study areas, the 

risk estimates have wide confidence intervals that can include zero, due to the lower statistical 

power of some of the city-specific effect estimates relative to the national combined effect 

estimate across cities. Furthermore, there is significant variability in these effect estimates across 

the 12 urban study areas, with some urban study areas having effect estimates from 5 to 7 times 

greater than other cites (see Chapter 7, section 7.4.1).7

 The variability in effect estimates, along 

with differences in O3 concentrations, is a driver for the overall variability in the risk results 

across urban study areas. Smith et al (2009) reports an overall significant national mortality 

effect estimate with confidence intervals that do not include zero, reflecting the much greater 

statistical power available when pooling information across urban study areas. 

We also evaluated mortality risks in the 12 urban study areas associated with long-term 

O3 exposures (based on the seasonal average (April to September) of the peak daily 1-hr 

maximum concentrations). Mortality risks from long-term exposures after just meeting the 

existing standard are substantially greater than risks from short-term exposures, ranging from 16 

to 20 percent of respiratory mortality across urban study areas. This compares with mortality 

 

7 This substantial heterogeneity in effect estimates can reflect a number of factors including differences in population 

susceptibility and behavior related to O3 exposure and risk (e.g., proximity to roadways, use of air conditioning, 

commuting patterns, time spent outdoors) and differences in the degree to which the O3 monitoring network used 

in the epidemiological study reflects patterns of population exposure. 
9-24 

risks from short-term exposures which range from 1 to 4 percent of total mortality. However, the 

percent reductions in long-term mortality risks are similar to those for mortality from short-term 

exposures. For example, we find less than or equal to 5 and 10 percent reductions in risk relative 

to just meeting the existing standard in most areas (excluding New York) when just meeting the 

70 ppb and 65 ppb alternative standards, respectively, and a less than 17 percent reduction when 

just meeting the 60 ppb alternative standard level. Risk reductions for the New York urban study 

area are much greater when just meeting the 65 ppb alternative standard compared to just 

meeting the existing standard, with a 24 percent reduction in risk in 2007. 

New York and Los Angeles have characteristics that make epidemiological risk estimates 

particularly uncertain. In the case of New York, the expansion of the urban study area definition 

to the CBSA adds uncertainty due to the large and diverse nature of the CBSA. The New York 

CBSA includes two urban study areas which have separate effect estimates available from the 

Smith et al. (2009) study. These separate effect estimates (for Newark, NJ and Jersey City, NJ) 

are smaller than the effect estimate for New York, however, they are also based on much smaller 

populations, and have relatively wider confidence bounds, reflecting low statistical power. For 

consistency with other urban study areas and to allow for comparison between the CBSA-based 

risk estimates and the smaller study area based estimates (see the sensitivity analyses in Chapter 

7), we elected to apply the New York city effect estimate, which is based on a very large 

population and has high precision, to all of the counties in the New York CBSA. While this adds 

substantial uncertainty to the absolute incidence of mortality for the New York CBSA, it does 

not affect the pattern of risk reductions when just meeting alternative standards. In addition, as 

noted earlier, the O3 adjustments to meet existing and alternative standards in New York and Los 

Angeles also have additional uncertainties relative to the other 10 urban study areas. 

We conducted a number of sensitivity analyses based on a population normalized 

mortality risk metric, e.g. mortality risk per 100,000 population. Maintaining the general linear, 

no-threshold functional form, mortality risks per 100,000 population are generally robust to 

alternative specifications of the C-R functions, although in several urban study areas, using effect 

estimates from Smith et al. (2009) which were derived using regional priors rather than national 

priors results in higher risk estimates.8

 Using the effect estimates from Zanobetti and Schwartz 

 

8

 In Bayesian modeling, effect estimates are “updated” from an assumed prior value using observational data. In the 

Smith et al (2009) approach, the prior values are either a regional or national mean of the individual effect 

estimates obtained for each individual city. The Bayesian adjusted city-specific effect estimates are then 

calculated by updating the selected prior value based on the relative precision of each city-specific estimate and 

the variation observed across all city-specific individual effect estimates. City-specific estimates are pulled 

towards the prior value if they have low precision and/or there is low overall variation across estimates. Cityspecific estimates are given less adjustment if they are precisely estimated and/or there is greater overall variation 

across estimates. 
9-25 

(2008) has no consistent effect on risk results across the urban study areas. Using effect estimates 

based on a co-pollutant model with PM10, mortality risks are higher in some locations and lower 

in others. However, in all locations the confidence intervals are substantially wider using the copollutant model with PM10 (due to fewer days with both pollutants measured), which makes it 

difficult to determine whether the increases and decreases in estimates relative to the core 

estimates are real or the result of statistical error. 

We selected the CBSA as the spatial definition for the urban study areas. We made this 

selection to address a downward bias that we identified resulting from a mismatch between the 

smaller urban core areas used in the epidemiology studies and the larger areas where O3

concentrations are expected to change as a result of meeting the existing and alternative standard 

levels (see Chapter 7). We included a sensitivity analysis evaluating the result of using a smaller 

geographic area including only the counties used in the epidemiology study. As expected, using a 

smaller geographic extent for the urban study areas results in smaller, and in some cases negative 

risk reductions when compared to using the CBSA definitions. This reflects the fact that the 

controlling monitor9 in many of the 12 urban study areas is located outside of the small set of 

counties included in the Smith et al. (2009) urban study area definitions, and some of the 

monitors that are within that more limited spatial extent are more prone to O3 titration due to 

local NOx emission sources. As a result, those monitors are more likely to see increases in O3

which will, if other monitors with higher concentrations in the broader regions are not included, 

lead to estimated increases in risk due to the application of a linear, no threshold C-R function. 

This bias can be substantial, especially in St. Louis and several urban study areas in the 

Northeast, including Boston, New York, and Philadelphia, where the highest concentration 

monitors are outside the Smith et al. (2009) urban study area definitions. 

Sensitivity analyses were conducted for scenarios of just meeting existing and alternative 

standards using combinations of NOx and VOC emissions reductions (as compared to NOx

reductions alone). The addition of VOC emissions reductions had little impact with the exception 

of New York and Los Angeles, where risk was decreased relative to the NOx-only reduction 

scenario. 

9.2.4.2 National-scale assessment results 

The national-scale assessment evaluated only mortality associated with recent O3

concentrations across the entire U.S for 2006-2008. The national-scale assessment is a 

complement to the urban scale analysis, providing both a broader geographic assessment of O3-

related health risks across the U.S., as well as an evaluation of how well the 12 urban study areas 

 

9

 The controlling monitor is the monitor with the highest design value within a defined non-attainment area. 
9-26 

represented the full distribution of O3-related health risks in the U.S. The national-scale 

assessment demonstrates that there are O3 risks across the U.S, not just in urban study areas, 

even though the O3 concentrations in many areas were lower than the existing standard level. 

While we did not assess the changes in risk at a national level associated with just meeting 

existing and alternative standards, just meeting existing and alternative standards would likely 

reduce O3 concentrations both in areas that are not meeting those standards and in locations 

surrounding those areas, leading to risk reductions that are not included in the urban-scale 

analysis. 

9.3 COMPARISON OF RESULTS ACROSS EXPOSURE, LUNG FUNCTION RISK, 

AND EPIDEMIOLOGY-BASED MORTALITY AND MORBIDITY RISK 

ANALYSES 

In considering the overall results across the human exposure, lung function risk, and 

epidemiology-based risk assessments, we focus on the key policy-relevant metrics and levels for 

each type of assessment. For the human exposure assessment, we selected exposures above the 

60 ppb exposure benchmark for all children (ages 5-18). We select this exposure metric because 

children represent a key at-risk lifestage, and the 60 ppb exposure benchmark is the lowest 

exposure level associated with significant findings in controlled human exposure studies. For the 

lung function risk assessment, we selected the results for lung function decrements greater than 

or equal to 10 percent for all children (ages 5-18). We select this lung function risk metric 

because children represent a key at-risk lifestage, and a 10 percent lung function decrement 

represents a potentially more adverse event in asthmatic children. For the epidemiology-based 

risk assessment we selected the core short-term exposure mortality results and the respiratory 

hospital admission results, because these endpoints were estimated for all of the 12 urban study 

areas. Generally speaking, these metrics provide the most differentiation between the alternative 

standards, helping to inform policy-relevant questions regarding adequacy of the existing 

standard, and public health impacts of meeting alternative standards. The other metrics analyzed 

in this HREA (e.g. other exposure benchmarks and other lung function decrements) show less 

response to just meeting the existing standard or potential alternative standard levels. 

As discussed in Chapter 2, we designed the exposure and risk assessment to help inform 

two fundamental questions related to the adequacy of the existing standard in protecting public 

health and the degree of exposure and risk reductions associated with alternative standards 

compared with the existing standard. The following discussion evaluates the three types of 

analyses we conducted in terms of the consistency of the information provided to inform these 

questions. 
9-27 

9.3.1 Evaluation of Exposures and Risks after Just Meeting the Existing Standard 

To compare the results of the three assessments in urban study areas, we plot the key 

metrics from each analysis across urban study areas for the two common years of analysis (i.e., 

2007 and 2009). For three urban study areas (i.e., Chicago, Dallas, and Washington D.C.) we 

have only the exposure and lung function risk assessments, as these urban study areas did not 

have sufficient information to estimate epidemiology-based risks. The epidemiology-based 

metrics are the percent of baseline short-term exposure mortality, based on the core estimates 

using the C-R functions from Smith et al. (2009), and respiratory hospital admissions based on 

the core estimates using the C-R functions from Medina-Ramon (2006), attributable to O3. 

Figure 9-7 presents the exposures and risks after just meeting the existing standard of 75 ppb. 

Each row represents one of the key analytical results; each column gives the results for 2007 and 

2009 for each urban study area. The scale of each analytical metric for each analysis differs, and 

thus the comparisons across analyses should focus on overall patterns rather than on direct 

comparisons of numeric estimates. 

All of the metrics show substantial variability among urban study areas, although there 

appears to be less variability in lung function risk and hospital admission risk compared with the 

exposure metric and mortality risk. The differences between estimates for 2007 and 2009 are 

much higher for some urban study areas (e.g., Baltimore and Philadelphia) for the exposure 

metric than any of the risk metrics. This may reflect the explicit threshold nature of the exposure 

metric, which focused on daily maximum 8-hr average exposures above a benchmark level of 60 

ppb. Differences between years in exposures at or above the 60 ppb benchmark after adjusting 

air quality to just meet the existing standard are dependent on the number of days during each 

year with decreases in higher O3 concentrations, as well as the magnitude of the decreases in O3

on those higher O3 concentration days. These in turn are sensitive to the shape of the O3

distribution in the analytical year prior to just meeting the existing standard (which determines 

the starting number of days above 60 ppb) and the response to emissions reductions applied in 

meeting the existing standard for 2007 or 2009. There is some consistency between metrics in 

the urban study areas with highest values for the exposure and lung function risk metrics. 

However, there were still differences, especially for Los Angeles, which had one of the higher 

values for lung function risk in 2009, but had one of the lower percentages of school-age 

children exposed at or above the 60 ppb benchmark. This again points to the importance of the 

threshold nature of the exposure metric, combined with the tendency for more substantial 

decreases in peak O3 concentrations relative to mid-range and low concentrations when adjusting 

air quality to just meet the existing standard. 

There is little consistency within urban study areas between the epidemiology risk 

metrics and the exposure and lung function risk metrics, and there is also little consistency 
9-28 

between the mortality and hospital admission risks. Houston has the lowest metric values in 2007 

(except for mortality risk), but in 2009 has some of the higher risk metrics (except for hospital 

admission risk). New York has the highest mortality risk in 2007 and 2009 but has among the 

lowest hospital admission risks in both years. 
9-29 

Figure 9-7. Comparison of Exposure (Row 1), Lung Function Risk (Row 2) and Epidemiology-Based Risk 

Metrics after Just Meeting the Existing 75 ppb Standard.

Atlanta Baltimore Boston Chicago Cleveland Dallas Denver Detroit Houston Los Angeles New York Philadelphia Sacramento 

0

1020

05

101520

012340123
9-30 

9.3.2 Reductions in Exposure and Risk Metrics after Just Meeting Alternative Standards 

To compare the results of the three assessments for urban study areas after adjusting air 

quality to just meet alternative standards relative to the existing standard, we express each result 

as a percent of the metric value when just meeting the existing standard. Figure 9-8 presents the 

percent reduction in exposures and risks after just meeting alternative standards relative to just 

meeting the existing standard of 75 ppb. In this plot, each row represents one of the key 

analytical results and each column gives the results for 2007 and 2009 for each urban study area. 

The scales are the same between analyses, and as such, it is informative to examine both the 

overall patterns of change between alternative standards, and also the absolute value of the 

percent reductions in risk metrics between analyses. In interpreting this chart, higher values 

mean greater reductions in risk or exposure relative to just meeting the existing standards. 

Because these are percent reductions, the maximum value is one hundred percent, which if 

reached would indicate that risks or benchmark exposures are completely eliminated when the 

alternative standard is met in the urban study area as was seen for the 60 ppb exposure 

benchmark. 

Many of the differences in results across the metrics are driven by how each metric is 

affected by the O3 data input to the analysis. In general, the impact of the HDDM adjustments to 

O3 vary based on three main considerations: (1) the degree to which the exposure or risk metric 

is sensitive to changes across the various ranges of O3 concentrations (e.g. high, mid-range, low); 

(2) whether the exposure or risk metric uses individual census tract concentrations or area-wide 

average concentrations; and (3) changes in the distribution of O3 concentrations in the year of 

analysis between recent O3 concentrations and adjusted (meeting the existing or alternative 

standards) O3 scenarios. With respect to consideration (1), the exposure benchmark metric, 

which focuses only on exposures above 60 ppb, will not be sensitive at all to changes in O3

concentrations in the range below 60 ppb. The lung function risk metric, which depends on the 

dose rate and individuals’ characteristics, does not have a concentration threshold. However, 

because of the logistic form of the response function, it is less sensitive to lower O3

concentrations and has very few FEV1 responses greater than 10 percent when exposure 

concentrations are below 20 ppb and very few FEV1 responses greater than 15 percent when 

exposure concentrations are below 40 ppb. On the other hand, the mortality and hospital 

admission risk metrics are based on non-threshold, approximately linear C-R functions, and 

therefore will be sensitive to changes in O3 along the full range of O3. As discussed in Chapter 4, 

because O3 at lower concentrations may increase following HDDM adjustment in some locations 
9-31 

and on some days to just meet alternative standards,10 this can lead to increases in risk on some 

days, which can lead to a net increase or decrease in risk over the entire year, depending on 

whether the days with increased risk exceed days with decreased risk (generally due to a 

preponderance of days with lower O3 concentrations). With respect to consideration (2), the 

exposure and lung-function risk metrics are based on concentrations at individual census tracts 

since they depend on O3 exposure modeled by moving each individual through their 

environment. Because of this, the exposure and lung-function risk metrics are most affected by 

the spatial and temporal variability of O3 concentrations across the urban study area. The 

mortality and hospital admission risk metrics are calculated applying C-R functions to area-wide, 

daily maximum 8-hr average O3 concentrations. As a result, the spatial variability in O3

concentrations between the monitors will only influence the epidemiology-based risk estimates 

in how they influence the area-wide average. With respect to consideration (3), all three metrics 

are influenced by how the distribution of O3 concentrations changes between recent O3

conditions and after adjustment to just meet existing and alternative O3 standard levels. 

The exposure and lung function risk metrics are most affected by the reductions in the 

individual monitors’ peak O3 concentrations, including the magnitude of these reductions and the 

number of days that experience these reductions. In contrast, the mortality and hospital 

admission risk metrics are affected by changes in the mean of the seasonal, area-wide average O3 

concentrations, where the mean is determined by the frequency and magnitude of increases 

versus decreases in area-wide, daily maximum 8-hr O3 concentrations.11 In addition to O3

concentrations, there are other factors that affect the variability across urban study areas for these 

three metrics, such as activity data and exposure factors for the exposure and lung function risk 

metrics and the study-specific C-R functions for the mortality and hospital admission risk 

metrics.

 

10 The frequency and magnitude of increases in spatially averaged mean concentrations in an urban study area occur 

during a season when adjusting air quality to just meet a standard vary considerably between the existing and 

alternative standards. The highest frequency of occurrence of days with increasing O3 happens when adjusting air 

quality to just meet the existing standards, and decreases as air quality is further adjusted to just meet lower 

alternative standard levels. 11 As noted previously, changes in the spatial extent of the urban study areas over which monitors are averaged can 

change the magnitude and sign of the change in the spatial average O3 concentration for an urban study area. For 

example, we found that we bias the risk estimates low when using urban study area definitions that include only 

urban core counties and not the counties with monitors experiencing the most reductions in O3.
9-32 

Figure 9-8. Comparison of the Percent Reduction in Key Risk Metrics for Alternative Standard Levels Re

Meeting the Existing 75 ppb Standard.

Atlanta Baltimore Boston Chicago Cleveland Dallas Denver Detroit Houston Los Angeles New York Philadelphia Sacramento St Louis 

0

255075

100

0

255075

100

0

255075

100

0

255075

100

2007 2009 2007 2009 2007 2009 2007 2009 2007 2009 2007 2009 2007 2009 2007 2009 2007 2009 2007 2009 2007 2009 2007 2009 2007 2009 2007 200

Analytical Year

% Reduction from Just Meeting Existing Standard 
9-33 

One clear observation is that the percent reductions in risk from meeting alternative 

standard levels relative to meeting the existing standard for the two epidemiology-based 

endpoints are much smaller than for the exposure benchmark and lung function risk endpoints. 

The maximum percent reduction in the mortality and hospital admissions risk relative to just 

meeting the existing standard across years, locations, and alternative standards is less than 25 

percent, and for many years/locations, the reductions in these risks when just meeting the lowest 

alternative standard, 60 ppb, are less than 10 percent. The exposure benchmark results show the 

most reductions when comparing just meeting the existing standard to just meeting alternative 

standards. Just meeting the 65 ppb standard results in reductions in the percent of children 

exceeding the 60 ppb exposure benchmark by over 50 percent in all urban study areas, and by 

over 75 percent in 12 of the 15 urban study areas evaluated. For most locations and years, just 

meeting the 60 ppb alternative standard reduced the percent of children exceeding the 60 ppb 

exposure benchmark by over 90 percent compared to just meeting the existing standard. 

Reductions in lung function risk were also much higher than reductions in mortality and hospital 

admissions risk. Air Quality just meeting the 65 ppb standard results in reductions in lung 

function risk by over 25 percent in most locations and years, and just meeting the 60 ppb 

standard results in reductions by over 40 percent in most locations and years. 

There is general consistency in the study area-to-study area patterns of reductions in the 

exposure and lung function risk metrics, although the decreases in lung function risk are less than 

half as large as the reductions in the percent of all school-age children exceeding the 60 ppb 

exposure benchmark (with the clear exception of the New York study area, which we will 

discuss further below). The patterns of reductions in mortality and hospital admission risk are 

generally consistent with the patterns for exposure and lung function risk for 2007, with the 

exception of Houston and Philadelphia. However, for 2009, the patterns for mortality and 

hospital admission risk are quite different, both from the 2007 results, and from the exposure and 

lung function risk results. This is due to the generally lower O3 concentrations in 2009, which 

results in a greater number of days with predicted increases in O3 concentrations at low 

concentrations, fewer days with very high concentrations where predicted reductions in O3 occur, 

and a smaller predicted decrease in O3 concentrations on those high days. This affects the 

mortality and hospital admissions risk more than the exposure and lung function risk metrics 

because those metrics incorporate thresholds, and therefore are not responsive to changes in O3

concentrations below those thresholds. 

Additional considerations are important in interpreting the reduction in exposure and risk 

between the existing standard and alternative standards. The HREA analyses focus on reducing 

peak O3 concentrations, in particular the 4th high O3 concentration averaged over 3-years so as to 

simulate meeting the existing standard or various alternative standards. In addition, the air 
9-34 

quality adjustments are based on applying reductions in U.S. anthropogenic emissions. In this 

way, the adjusted air quality reflects day-to-day O3 concentrations that could occur when 

focusing on reducing high O3 concentrations rather than on reducing mean O3 concentrations. In 

addition, because the analyses do not include reductions of O3 precursor emissions from sources 

other than U.S. anthropogenic emissions (e.g. international emissions, biogenics, etc), the O3

concentrations in the adjusted air quality account for O3 created from natural and international 

sources, even if 100 percent emissions reductions are applied to U.S. anthropogenic sources in 

adjusting air quality scenarios. 

Finally, with respect to the epidemiology based analyses, we note that 2007, which had 

generally higher O3 concentrations than 2009, had more days where O3 concentrations decreased 

as a result of adjusting peak O3 concentrations to just meet alternative standards. Thus just 

meeting alternative standards resulted in net decreases in risk in all locations, with the exception 

of Houston for just meeting the 70 ppb alternative standard. In contrast, 2009, which had 

generally lower concentrations than 2007, had more days in the range where O3 concentrations 

were increased as a result of adjusting peak O3 concentrations to just meet alternative standards, 

and thus the patterns reflect some locations where mortality and hospital admissions risk 

increases. However, for 2009, in all locations, when just meeting the lowest alternative standard 

of 60 ppb, mortality and hospital admission risks are decreased relative to just meeting the 

existing standard. 

9.4 OVERALL ASSESSMENT OF REPRESENTATIVENESS OF EXPOSURE AND 

RISK RESULTS 

9.4.1 Representativeness of Selected Urban Study Areas in Reflecting Area across the 

Nation with Elevated Risk 

We selected urban study areas for the exposure and risk analyses based on several criteria 

(e.g. recent elevated O3 concentrations and presence of at-risk populations and lifestages) we 

identified as likely indicators of areas and populations likely to experience high O3 exposures 

and risks (see Section 7.3.1). We then conducted several analyses to determine the extent to 

which our selected urban study areas actually represent the highest mortality and morbidity risk 

areas. We compared the distributions of risk characteristics12 and mortality risk (based on recent 

O3 concentrations) for the 12 urban study areas used in the epidemiology-based risk assessment 

with the corresponding national distributions. We also evaluated the degree to which our selected 

 

12 In this context, risk characteristics are the elements of populations, air quality, and inputs to the C-R functions that 

are expected to be correlated with estimated mortality risks (see Chapter 8). 
9-35 

urban study areas represent the patterns of O3 concentration changes experienced by the overall 

U.S. population. 

Based on the comparisons of distributions of risk characteristics, the selected urban study 

areas represent urban study areas that are among the most populated in the U.S., have relatively 

high peak O3 concentrations, and capture well the range of city-specific mortality risk effect 

estimates. These three factors alone would suggest that the urban study areas should capture well 

the overall risk for other heavily populated urban study areas in the nation, with a potential for 

better characterization of the high end of the risk distribution. The selected urban study areas do 

not include those with the highest numbers of some at-risk populations or lifestages, specifically 

older people with high baseline mortality rates. However, most locations in the U.S. (except 

Florida) with high percentages of older people have low overall populations, less than 50,000 

people in a county, or low O3 concentrations. This suggests that while the risk per exposed 

person per ppb of O3 may be higher in these locations, the overall risk to the population is likely 

to be within the range of risks represented by the urban study locations. 

Based on the comparisons of distributions of short-term O3 exposure mortality risk (using 

the percent of mortality metric) for recent O3 concentrations, the 12 selected urban study areas 

are representative of the full distribution of U.S. O3-related mortality risk in urban study areas. 

Two of the selected areas, New York and Philadelphia are representative of the highest end of 

the distribution of short-term O3 mortality risk. Overall, O3 mortality risk for short-term O3

exposures in the 12 urban study areas are representative of the full distribution of U.S. urban O3-

related mortality, representing both high end and low end risk counties. For the long-term O3

exposure mortality risk metric (again using the percent of mortality), the 12 urban study areas are 

representative of the central portion of the distribution of risks across all U.S. counties; however, 

the selected 12 urban study areas do not capture the very highest (greater than 98th percentile) or 

lowest (less than 25th percentile) ends of the national distribution of long-term exposure-related 

O3-related risk. 

9.4.2 Representativeness of Selected Urban Study Areas in Reflecting Responsiveness of 

Risk to Just Meeting Existing and Alternative O3 Standards 

While we selected urban study areas to represent those populations likely to experience 

elevated risks from O3 exposure, we did not include among the selection criteria the 

responsiveness of O3 in the urban study area to decreases in O3 precursor emissions that would 

be needed to just meet existing or alternative standards. 

 In our preliminary evaluations of risk modeling results, we observed a consistent 

presence of days with low to midrange starting O3 concentrations for which O3 concentrations 

(using the 8-hr maximum metric) increased after adjustments to just meet the existing and 
9-36 

alternative standards across the selected urban study areas. As noted above, this led to estimates 

of increased risk on those days, and in some cases, estimates of increased risk over the course of 

the O3 season, reflecting both the magnitude and frequency of the predicted increases relative to 

the predicted decreases in O3 concentrations. As explained above, this pattern was more 

pronounced when using a more spatially limited definition of the urban study areas, but even 

when using the CBSA definitions, there were still days when the area-wide average O3 increased, 

primarily due to predicted increases in O3 in the core counties of the urban study areas. 

 In order to better understand how prevalent this type of air quality response was across 

the U.S., we conducted several additional analyses of O3 concentrations. These included 

evaluations of trends at O3 monitors during a period of time with significant O3 precursor 

emission reductions, and evaluations of temporal and spatial patterns of O3 changes across the 

U.S., based on air quality modeling results, to simulate how O3 would change across the U.S. in 

response to NOx (and VOC) emissions reductions (relative to recent 2007 levels) similar to those 

used in the HDDM adjustments (see section 9.2.1 above). The latter analysis includes an 

assessment of the association of different types of O3 responses with population counts to help 

characterize the degree to which populations in the U.S. experience O3 conditions like those in 

the selected 15 urban study areas (see Chapter 8). 

Overall, both types of analyses showed that decreases in O3 precursor emissions lead to 

decreases in O3 concentrations in areas with higher starting O3 concentrations, which tend to be 

rural or suburban study areas, and on days with higher O3 concentrations. The analyses also 

indicate that in urban core areas (those with high levels of fresh NOx emissions), decreases in 

NOx emissions can lead to increases in O3, primarily for days when initial O3 concentrations are 

suppressed due to NOx titration. This is consistent with conclusions of the O3 ISA (U.S. EPA, 

2013, Sections 3.2.4, 3.6.2.1) that O3 can be suppressed in high NOx environments. The 

observed widespread decreases of median O3 in suburban and rural locations when NOx

emissions are decreased suggest the efficacy of large NOx emissions reductions on reducing O3

over large regions of the country. 

These results suggest that many of the urban study areas may show O3 responses that are 

typical of other large urban study areas in the U.S., but may not represent the response of O3 in 

other populated areas of the U.S., including suburban study areas, smaller urban study areas, and 

rural areas. These smaller urban study areas would be more likely than our urban study areas to 

experience area-wide average decreases in mean O3 concentrations as O3 standards are met. Even 

though large urban study areas throughout the U.S. have high population density, 73 percent of 
9-37 

the U.S. population lives outside of these high population density areas13, and thus, a large 

proportion of the population is likely to experience greater mortality and morbidity risk 

reductions in response to reductions in 8-hr O3 concentrations than are predicted by our modeling 

in the selected urban study areas. The analyses presented in Section 8.2.3.2 show that 

populations in the study areas we selected are approximately twice as likely to experience 

increasing mean O3 concentrations as populations in the U.S. as a whole. Because our selection 

strategy for risk modeling was focused on identifying areas with high risk, we tended to select 

large urban population centers. As discussed in the previous section, this strategy was largely 

successful in including those urban study areas in the upper end of the O3 risk distribution. 

However, this also has led to an overrepresentation of the populations living in locations where 

we estimate increasing mean seasonal O3 in response to adjusting air quality to just meet the 

existing and alternative standards using NOx emissions reductions. The implication of this is that 

our estimates of mortality and morbidity risk reductions for the selected urban study areas are 

likely to understate the average risk reduction that would be experienced across the population 

and should not be seen as representative of potential risk reductions for most of the U.S. 

population. 

9.5 OVERALL ASSESSMENT OF CONFIDENCE IN EXPOSURE AND RISK 

RESULTS 

As with any complex analysis using estimated parameters and inputs from numerous data 

sources and models, there are many sources of uncertainty that may affect our exposure and risk 

estimates. These sources of uncertainty are discussed in each of the chapters related to air 

quality, exposure, lung function risk, and epidemiology based mortality and morbidity risk. The 

overall effect of the combined set of uncertainties on confidence in the interpretation of the 

results of the analyses is difficult to quantify. However, we provide our judgment of our overall 

confidence here, with an understanding that alternative judgments may also be supported. 

The degree to which each analysis was able to incorporate quantitative assessments of 

uncertainty differed, due to differences in available information on uncertain parameters and 

complexities in propagating uncertainties through the models. In general, we followed the World 

Health Organization tiered approach to uncertainty characterization (WHO, 2008), which 

includes both quantitative and qualitative assessments. Each chapter includes a table identifying 

and characterizing the potential impact of key uncertainties on risk estimates, including the 

degree to which we were able to quantitatively address those uncertainties. 

 

13 High population density areas are defined here as locations with population densities greater than 1000 

people/km2

.
9-38 

In considering our overall confidence in the results, there are several key considerations 

discussed below related to sources of uncertainty which we were not able to fully quantify, but 

which may have a large impact on both overall confidence and confidence in individual analyses. 

9.5.1 Uncertainties in Modeling Ozone Responses to Meeting Standards 

There is inherent uncertainty in all deterministic air quality models, such as CMAQ, the 

photochemical grid model used to develop the model-based O3 adjustment methodology. 

Evaluations of air quality models against observed pollutant concentrations build confidence that 

the model performs with reasonable accuracy despite both structural and parametric 

uncertainties. A comprehensive model performance evaluation provided in Appendix 4-B shows 

generally acceptable model performance that is equivalent to or better than typical state-of-the 

science regional modeling simulations described in Simon et al. (2013). Two additional sources 

of uncertainties in the HDDM adjustment methodology are the applicability of HDDM 

sensitivities over large emissions perturbations and the variability in data used to create 

regressions which allowed the application of these sensitivities to ambient data. 

Both sources of uncertainty are shown to be reasonably small in chapter 4 with the first 

having a mean error of less than 1ppb for 50% NOx cuts and less than 4 ppb for 90% NOx cuts. 

The regressions, which were developed to relate O3 response to emissions perturbations with 

ambient O3 concentrations for every season, hour-of-the-day, and monitor location, are purely 

empirical so applying O3 responses to ambient data based on this modeled relationship adds 

uncertainty. Preliminary work showed that the relationships developed with these regressions 

were generally statistically significant for most season, hour-of-the-day, and monitor location 

combinations for 2005 modeling in Detroit and Charlotte (Simon et al, 2013). Despite the 

empirical nature of the regressions, the statistically significant fits and the operational evaluation 

of the model which shows satisfactory ability of the model to predict changes in ozone under 

varying meteorology and emissions conditions (Appendix 4-B) build confidence in the 

application of these modeled relationships to ambient data. The uncertainty introduced from the 

application of regressions to determine sensitivities were quantified by propagating uncertainties 

in the sensitivities through to uncertainties in the final predicted O3 concentrations which had 

standard errors less than 1.4 ppb for all adjustment scenarios. New York and Los Angeles had 

the largest uncertainties in these two areas due to the fact that they required the largest reductions 

in NOx emissions. Uncertainties stemming from the application of 8-months of model data to 5-

years of ambient data and the across-the-board emissions cut assumptions are further discussed 

in chapter 4 but are not expected to substantially degrade confidence in the air quality results. 
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9.5.2 Uncertainties in Modeling Exposure and Lung Function Risk 

With regard to the exposure and lung-function risk estimates, the modeling explicitly 

incorporates population variability in many of the modeling inputs. We did not attempt to 

probabilistically incorporate the many sources of uncertainty in model parameters or input data 

due to limitations in the ability to specify distributions characterizing our confidence in those 

variables. To explore the impacts of some of the more important sources of uncertainty, we 

conducted a limited set of sensitivity analyses. For the exposure assessment, the estimate of 

repeated exposures above exposure benchmarks is based on the limited set of diaries of activity 

data available in the Consolidated Human Activity Database (CHAD) database (see Chapter 5). 

The method for constructing activity patterns over the course of an O3 season may not fully 

capture the behavior of children who have systematically high outdoor activity levels. As a 

result, while we are able to report the percent of children with two or more exposures, modeling 

of the distribution of multiple exposures is limited, and the ability to identify the percent of the 

population with unusually high numbers of multiple exposures is not possible. 

For the lung function risk assessment, sensitivity analyses indicate that the MSS model 

parameter related to the impact of the ventilation rate was most influential in determining the 

estimated number of children with FEV1 decrements greater than 10 percent. Estimates of lung 

function decrements are also influenced by how much variability in individual response is 

assumed in the MSS model. Sensitivity analyses indicate that when a greater amount of 

variability is allowed in the MSS model, the percent of children ages 5-18 with FEV1 decrements 

greater than 10 percent can increase substantially. In addition, we performed analyses to 

understand the age-related factors in APEX that could influence the estimated FEV1 decrements. 

It was found that the four most influential factors influencing the relationship between the 

predicted FEV1 decrement and age are the decreasing level of exertion, the decreasing equivalent 

ventilation rate (with increasing age), the higher time spent outdoors by children, and the higher 

exposure concentration experienced by children while outdoors. These all lead to children having 

higher FEV1 decrements than adults, and are more influential than the MSS model age term. 

9.5.3 Uncertainties in Modeling Epidemiological-Based Risk 

A major issue in using the results of the epidemiology studies in estimating risk is the 

narrow geographic definition used for urban study areas in the epidemiology studies. In many of 

the urban study areas, we observe two distinct patterns of O3 response to the reductions in 

precursor emissions we evaluated to just meet the existing and alternative standard levels. The 

first pattern generally occurs in areas outside the urban core (e.g. suburban and rural areas), and 

on days when O3 concentrations are on the higher end of the distribution of O3 concentrations, 

and is characterized by predicted decreases in 8-hr O3 concentrations. These tend to be the 
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locations where the highest 8-hr design values occur. The second pattern generally occurs in the 

urban core, and on days when O3 concentrations are on the lower end of the distribution of O3

concentrations, and is characterized by predicted increases in 8-hr O3 concentrations. The narrow 

definitions of urban study areas used in the epidemiological studies generally included the urban 

core areas, but did not include all of the suburban or rural areas. The narrow geographic 

definitions led to a clear downward bias in the estimates of risk changes that would be associated 

with just meeting the standards in the urban study areas, because the risk changes would reflect 

the locations with a tendency towards increases in 8-hr O3, but would not include locations 

outside the urban core with decreases in O3. In many cases, the narrowly defined geographic 

definitions used in the epidemiology studies did not even include the location with the monitor 

that was violating the standard. We addressed this bias by expanding the urban study area to the 

CBSA. However, this adds additional uncertainty to the risk estimates, and reduces our 

confidence that we have a good match between the basis of the C-R function (just urban core 

locations) and the risk analysis context (including both urban core counties and other counties in 

the CBSA). A clear implication of this decision is that the absolute incidence estimates will be 

larger than if the analysis was limited to a smaller number of counties. For this reason, we have 

placed more emphasis on risk metrics that have been normalized for population size (e.g. risks 

per 100,000 population and percent risk), so as to facilitate comparisons between study areas of 

different population sizes and to reduce the influence of population size on the risk metrics. 

The epidemiology studies used as the source for C-R functions for short-term exposure 

mortality and morbidity endpoints all use time-series approaches to estimate the effect of daily 

variations in O3 concentrations on daily mortality or morbidity incidence. The effect estimates 

developed in these epidemiology studies were based on air quality and health information 

observed from 1987-2000. These effect estimates were based on day-to-day variations in areawide observed O3 ambient monitoring concentrations that reflect a specific set of emissions and 

atmospheric conditions. In our analyses, we apply these effect estimates to adjusted air quality 

scenarios that are reflective of substantial changes in O3 concentrations across an area due to, in 

some cases, large decreases in NOx and VOC emissions reductions. The resulting spatial and 

temporal patterns of O3 modeled here may not be the same as the spatial and temporal patterns of 

O3 that existed at the time of the epidemiology study. The potential for different spatial and 

temporal patterns in O3 concentrations between the adjusted air quality scenarios and the air 

quality observed during the epidemiology study period potentially adds uncertainty to the 

estimates of risk, as it is not clear the degree to which the exposure surrogate used in the 

epidemiology study correlates with the exposure surrogate used in the risk analysis. However, 

the impact of these differences in temporal and spatial patterns is not likely to be great, and is 

likely to be less than other sources of uncertainty in the analysis. The use of Bayesian adjusted 
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effect estimates in the C-R functions for each urban study area should make each individual C-R 

function less sensitive to the particular spatial-temporal pattern present during the place and time 

used for the epidemiological analysis. 

There is also additional uncertainty in the specific quantitative estimates of mortality risk 

from long-term O3 exposures resulting from applying the non-threshold, two-pollutant model 

from Jerret et al. (2009). The results of a sensitivity analysis evaluating alternative threshold 

models showed that these mortality risk estimates are highly sensitive to the specific threshold 

concentration. Given that the authors of the Jerrett et al (2009) study concluded that there was 

substantial uncertainty about both the existence and level of a potential threshold, we 

acknowledge that there is substantially more uncertainty in the estimates of mortality associated 

with long-term exposures compared to those associated with short-term exposures. 

9.6 OVERALL INTEGREATED CHARACTERIZATION OF RISK IN THE 

CONTEXT OF KEY POLICY RELEVANT QUESTIONS 

Our analyses set out to inform two questions: (1) what are the magnitudes of exposures of 

concern and risks for O3-related health effects that are estimated to occur with O3 concentrations 

that just meet the existing O3 standard?; and (2) to what extent do alternative standards reduce 

estimated exposures and risks of concern attributable to O3, focusing on at-risk populations and 

lifestages? In evaluating risk, we did not limit the assessment to just the absolute risk that is 

attributable to U.S. or North American emissions, as this is not relevant to answer the two 

questions. Instead, we estimated total risk from all O3 concentrations and the distribution of risk 

over the range of O3 concentrations. Our estimates of changes in risk from meeting alternative O3

standard levels relative to meeting the existing standard reflect only the impact of reductions in 

U.S. precursor emissions on O3 distributions, recognizing that these emissions are most likely to 

be affected by implementation of the standards. 

To inform these questions, we conducted air quality, exposure, and risk analyses for 

selected urban study areas. We evaluated changes in the distribution of O3 concentrations along 

the full range of O3 concentrations down to zero. We have utilized a new method (compared to 

the O3 NAAQS review completed in 2008) for estimating O3 concentrations consistent with just 

meeting existing and alternative standards, based on modeling the response of O3 concentrations 

to reductions in U.S. anthropogenic NOx and VOC emissions, using the HDDM capabilities in 

CMAQ. This modeling incorporates all known emissions, including emissions from nonanthropogenic sources and anthropogenic emissions from sources in and outside of the U.S. As a 

result, background O3 concentrations are directly modeled and, therefore, do not need to be 

separately specified. Application of this approach also addresses the recommendation by the 

National Research Council (NRC, 2008) to explore how emissions reductions might affect 
9-42 

temporal and spatial variations in O3 concentrations, and to include information on how NOx

versus VOC control strategies might affect exposure to O3 and potential risks. 

We estimated exposures and risks using several different metrics. Consistent with the 

available evidence, we estimated the percentages of different study populations and lifestages 

with exposures exceeding several health-based exposure benchmarks. We estimated lung 

function risks based on a model of individual risk of lung function decrements that incorporates a 

dose-equivalent threshold and individual exposures, activity levels, and physiology. We 

estimated mortality and morbidity risks based on non-threshold C-R functions derived from 

epidemiology studies. These three different analyses result in differing sensitivities of results to 

changes in the O3 concentration distribution. Because the three metrics are affected differently in 

the analyses by changes in O3 at low concentration levels, it is important to understand these 

changes in O3 at low concentrations in interpreting differences in the results across metrics. 

We also evaluated the degree to which exposures of concern and lung function risk were 

reduced in the portions of urban study areas (urban core areas) that were more likely to 

experience an increase in low concentrations of O3, and in some cases an overall net increase in 

epidemiology based mortality and morbidity risk (results for this assessment are presented in 

Appendix 9A). We compared these estimates of changes in exposures and lung function risk to 

estimates of changes in exposures and lung function risk in the areas outside of the urban core 

areas to judge whether for exposures of concern and lung function risk we see the same pattern 

of risk reduction between those areas. 

Both exposures of concern and lung-function risk estimates in the core urban study areas 

showed similar patterns compared with the areas outside the urban cores when just meeting the 

existing and potential alternative standards. Thus, we observe that in urban core areas which in 

some cases showed overall increases in epidemiology-based mortality and morbidity risk when 

looking across these same air quality scenarios (see section 9.5.3), we generally see reductions in 

exposures of concern and lung function risk. These findings illustrate that populations within 

core urban study areas are likely to experience risk reductions for health endpoints reflected in 

the exposure and lung function analyses. 

The mortality and morbidity risk assessment is the analysis that is most sensitive to the 

increases in O3 in the lower part of the distribution of initial O3 concentrations at some monitors 

and on some days after meeting the existing and alternative standards in some urban study areas. 

As demonstrated in the heat maps (Figures 7-2 and 7-3), the increases in O3 (and resulting 

estimated increases in risk) occur largely on days with initial O3 concentrations in the range of 10 

to 40 ppb. In addition, mean O3 concentrations for the urban study areas change little between 

air quality scenarios for meeting the existing and alternative standards, because mean 

concentrations reflect both the increases in O3 at lower concentrations and the decreases in O3
9-43 

occurring on days with high O3 concentrations. This leads to small net changes in mortality and 

morbidity risk estimates for many of the urban study areas. For New York, we find there is a 

larger decrease relative to other urban study areas (nearly five times as large as the next largest 

result for Los Angeles), in mortality and respiratory hospital admissions when just meeting the 

65 ppb alternative standard compared to just meeting the existing standard, reflecting the large 

degree of air quality adjustment needed to meet the standard at all monitors in New York. Both 

the net change in risk and the distribution of risk across the range of O3 concentrations in the 

urban study areas may be relevant in considering the degree of additional protection provided by 

just meeting existing and alternative standards. 

The dampened response of short-term mortality risk can be contrasted with lung function 

risk estimates based on application of results from controlled human exposure studies. The lung 

function risk estimates primarily reflect changes in the upper end of the O3 distribution and 

reflect counts of exceedances of lung function decrement benchmarks, rather than summing risks 

across all days in the season. In addition, lung function risks are based on detailed 

microenvironmental exposure modeling that uses tract-level concentrations instead of composite 

monitor values, thereby resulting in less dampening of spatial variability in O3 within a given 

urban study area. 

The exposure benchmark analysis is the least sensitive to changes in O3 in the lower part 

of the distribution of initial O3 concentrations, because the lowest of the exposure benchmarks is 

60 ppb, well above the portion of the distribution where initial O3 concentrations tended to 

increase. Since the modeled exposures will always be less than or equal to the ambient 

concentrations, a benchmark of exposure at 60 ppb is above the range of O3 concentrations 

where the HDDM approach estimates increases in concentrations. Thus, this metric is most 

reflective of the decreases in O3 at high concentrations that are expected to result from just 

meeting the existing and alternative standards. 

The lung function risk analysis is less sensitive than the epi-based risk assessments to 

increases at very low concentrations of O3, because the epi-based risk function is logistic and 

shows little response at lower O3 dose rates that tend to occur when ambient concentrations are 

lower (generally less than 20 ppb for the 10 percent FEV1 decrement and generally less than 40 

ppb for the 15 percent FEV1 decrement). However, because there are still some increases in O3

concentrations that occur in the 50 to 60 ppb range where the estimated risk is more responsive, 

there may be some reduction in the magnitude of the risk decrease (this is evident when 

comparing the lung function risk metric with the exposure benchmark metric in Figure 9-7). 

The exposure-based lung function risk assessment is based on controlled human exposure 

studies which studied responses in healthy adults. Although the lung function model based on 

this population shows less responsiveness at lower ambient concentrations, the applicability of 
9-44 

this model to the responses of more sensitive populations and lifestages, including children and 

asthmatics, is uncertain. In addition, although the most complete information for generating an 

E-R function is available for FEV1 as a measure of lung function, there are other, potentially 

more public health relevant effects, such as lung inflammation, which have also been shown to 

respond to O3. As such, the lung function risk analysis should be seen as providing useful but not 

complete information on risks of health responses to O3. 

Exposures above health benchmarks and risks remain after adjusting O3 to just meet the 

existing standard. The percentage of children with at least one 8-hr O3 exposure exceeding 60 

ppb is greater than 10 percent in at least one of the five analytical years for all of the 15 urban 

study areas. The percent of children with a predicted decrement in lung function greater than or 

equal to 10 percent is greater than 16 percent in at least one of the five analytical years for all of 

the 15 urban study areas, and for a 15 percent decrement is less than 7 percent for all years and 

areas. O3-attributable mortality is slightly less than one percent up to four percent of total 

mortality across the 12 urban study areas, with little variation between 2007 and 2009. O3-

attributable respiratory hospital admissions are between 2 and 3 percent across the 12 urban 

study areas, with little variation between 2007 and 2009. The percent attributable risk for other 

morbidity endpoints is somewhat higher than for respiratory hospital admissions, but we only 

estimated these endpoints for a more limited set of urban study areas due to data limitations. 

The degree of reduction in exposures and risks when adjusting O3 from just meeting the 

existing standard to just meeting lower alternative standard levels varies considerably between 

metrics. The greatest degree of reduction occurs in exposures above the 60 ppb exposure 

benchmark, followed by reductions in lung function decrements greater than or equal to 10 

percent, with the smallest changes in mortality and respiratory hospital admissions. Although the 

magnitude of reduction differs between the different exposure and risk metrics, there are 

generally the same patterns of reductions for the exposure benchmark and lung function risk 

metrics, showing consistent reductions across all 15 urban study areas. Risk reductions also 

occur in most of the urban study areas for mortality and respiratory hospital admissions. 

However, these reductions are small, and reflect net changes in risk that include days with risk 

increases as well as risk decreases. For most urban study areas, the greatest incremental 

reductions in exposures above the 60 ppb benchmark occurred when just meeting 70 ppb 

compared to just meeting the existing standard. Just meeting lower standards of 65 ppb and 60 

ppb had incrementally smaller reductions in the percent of children exposed above 60 ppb. 

Incremental lung function risk reductions are more even between alternative standards, with 

similar or greater incremental reductions for the 65 ppb and 60 ppb alternatives compared with 

the incremental reductions for just meeting 70 ppb. Incremental reductions in mortality and 

respiratory hospital admissions risk are small between alternative standards, but more urban 
9-45 

study areas have somewhat larger risk reductions when comparing just meeting the 60 ppb 

alternative to just meeting the 65 ppb standard, than when comparing 65 ppb to 70 ppb or 70 ppb 

to 75 ppb. Long-term exposure mortality risk results show larger absolute estimates of mortality 

risk and more consistent reductions across urban study areas. However, percent changes in longterm exposure mortality are similar to those for short-term exposure mortality. 

In conclusion, we have estimated that exposures and risks remain after just meeting the 

existing standards and that in many cases, just meeting alternative standard levels results in 

reductions in those exposures and risks. Meeting alternative standards has larger impacts on 

metrics that are not sensitive to changes in lower O3 concentrations. When meeting the 70, 65, 

and 60 ppb alternative standards, the percent of children experiencing exposures above the 60 

ppb health benchmark falls to less than 20 percent, less than 10 percent, and less than 3 percent 

in the worst O3 year for all 15 study urban study areas, respectively. Lung function risk also 

drops considerably as lower standards are met. When meeting the 70, 65, and 60 ppb alternative 

standards, the percent of children with lung function decrements greater than or equal to 10 

percent falls to less than 21 percent, less than 18 percent, and less than 14 percent in the worst O3

year for all 15 urban study areas, respectively. When meeting the 70 and 65 ppb alternative 

standards, mortality risk attributable to short-term O3 exposures falls by up to 5 percent and up to 

22 percent, respectively across all 12 urban study areas, and when meeting the 60 ppb alternative 

standards, falls by up to 14 percent, excluding New York, where we were unable to adjust air 

quality to meet the 60 ppb alternative standard level. 

While there remain uncertainties in each of the analytical areas, we have sufficient 

confidence in the overall results for them to be useful in informing the policy assessment. Our 

assessment suggests that the highest confidence should be placed in the results of the human 

exposure and lung function risk results, largely because they are based on results of controlled 

human exposure studies and a physiology-based risk model. Medium to high confidence should 

be placed in the results of the assessment of epidemiology-based risks associated with short-term 

O3 exposures, because while the large number of studies supporting the C-R relationships used 

provides increased confidence, there remain uncertainties related to unexplained heterogeneity 

between locations, exposure measurement errors, and interpretation of the shape of the C-R 

function at lower O3 concentrations. Lower confidence should be placed in the results of the 

assessment of epidemiology-based mortality risks associated with longer-term O3 exposures, 

primarily because that analysis is based on only one well designed study, and because of the 

uncertainty in that study about the existence and location of a potential threshold in the C-R 

function. 

 
9-46 

9.7 REFERENCES 

Frey, C. and J. Samet. 2012. CASAC Review of the EPA’s Policy Assessment for the Review of 

the Ozone National Ambient Air Quality Standards (First External Review Draft – 

August 2012). U.S. Environmental Protection Agency Science Advisory Board. EPACASAC-13-003. 

Medina-Ramon, M.; A. Zanobetti and J. Schwartz. 2006. The effect of O3 and PM10 on hospital 

admissions for pneumonia and chronic obstructive pulmonary disease: a national 

multicity study.American Journal of Epidemiology. 163(6):579-588. 

McDonnell, W.F.; P.W. Stewart; M.V. Smith; C.S. Kim C.S. and E.S. Schelegle. 2012. 

Prediction of lung function response for populations exposed to a wide range of O3

conditions. Inhalation Toxicology. 24:619-633. 

Simon, H.; K.R. Baker; F. Akhtar; S.L. Napelenok; N. Possiel; B. Wells and B. Timin. 2013. A 

direct sensitivity approach to predict hourly O3 resulting from compliance with the 

National Ambient Air Quality Standard. Environmental Science and Technology. 

47:2304-2313. 

Smith, R.L.; B. Xu and P. Switzer. 2009. Reassessing the relationship between O3 and shortterm mortality in U.S. urban communities. Inhalation Toxicology. 21:37-61. 

U.S. EPA. 2007. Ozone Health Risk Assessment for Selected Urban Case Study Areas. Research 

Triangle Park, NC: Office of Air Quality Planning and Standards. (EPA document 

number EPA 452/R-07-009). 

<http://www.epa.gov/ttn/naaqs/standards/O3/s_O3_cr.html>. 

U.S. EPA. 2013. Integrated Science Assessment for O3 and Related Photochemical Oxidants: 

Final. Research Triangle Park, NC: U.S. Environmental Protection Agency. (EPA 

document number EPA/600/R-10/076F). 

World Health Organization. 2008. Part 1: Guidance Document on Characterizing and 

Communicating Uncertainty in Exposure Assessment, Harmonization Project Document 

No. 6. Published under joint sponsorship of the World Health Organization, the 

International Labour Organization and the United Nations Environment Programme. 

WHO Press, World Health Organization, 20 Avenue Appia, 1211 Geneva 27, 

Switzerland. 

Zanobetti, A. and J. Schwartz. 2008. Mortality displacement in the association of ozone with 

mortality: an analysis of 48 cities in the United States. American Journal of Respiratory 

and Critical Care Medicine. 177:184-189. 

 
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